ent Otitis by mikeholy

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Johannes Borgstein
The Basic ENT


                     johannes borgstein
        The Basic ENT

for A

Introduction............................................................ 9

A Few Historical Considerations ............................ 13

EQUIPMENT ......................................................... 17

BASIC DIAGNOSTIC PROCEDURES ........................ 21

a. OTOSCOPY ...................................................... 21

b. TUNING FORK TESTS (Weber & Rinne) .............. 24

c. VESTIBULAR TESTING ......................................... 27

d. RHINOSCOPY.................................................... 31

e. ORAL CAVITY EXAMINATION .............................. 33

f. INDIRECT LARYNGOSCOPY ................................ 34

g. POSTNASAL SPACE EXAMINATION ...................... 38

h. NECK EXAMINATION .......................................... 39

i. CRANIAL NERVES ............................................... 41

                                                        The Basic ENT


- Airway, Intubation, Cricothyroid puncture, Tracheotomy
EMERGENCY TRACHEOTOMY................................. 70

AND DIGESTIVE TRACT ......................................... 75

3. EPISTAXIS ........................................................ 81
TREATMENT OF EPISTAXIS...................................... 83
CAUTERY .............................................................. 83
PACKS .................................................................. 83
INJECTIONS........................................................... 87
SURGICAL LIGATION ............................................ 88

4. FOREIGN BODIES ........................................... 91

5. EAR PAIN (OTALGIA)....................................... 99

6. OTITIS ........................................................... 101

7. VERTIGO AND DIZZINESS............................... 115

8. DEAFNESS OR HEARING LOSS? ...................... 123

9. FACIAL PARALYSIS .......................................... 129

10. NASAL OBSTRUCTION................................... 133

11. SINUSITIS ..................................................... 135

12. HEADACHE .................................................. 139

13. HOARSENESS OR DYSPHONIA ..................... 143

14. TONSILLITIS & ADENOIDS ............................ 149

15. TUMOUR IN THE NECK ................................. 155
THE THYROID NODULE ........................................ 156

16. NASAL FRACTURES........................................ 159

17. DYSPHAGIA ................................................. 163

PROBLEMS IN CHILDREN .................................... 165

Index ................................................................. 169
The Basic ENT


        This is an introduction to Ear, nose and
Throat problems for Medical students, though
specialists or residents from related specialties
may find useful comments, hints and sugges-
     Upper airway problems (and the middle
ears form part of the upper airways) constitute
as much as 30% of all medical problems seen
by the general practitioner. Generally too lit-
tle time and attention is paid to this important
area, which is often dispensed with in a couple
of weeks.
     This book was written with the under-
standing that high-tech medicine is making
itself inaccessible to a large proportion of the
world’s population,
      I have tried to avoid as far as possible the
use of expensive equipment and studies, con-
                                     The Basic ENT

centrating more on clinical aspects and proce-
dures which do not necessarily require costly
and fragile equipment.
     After a discussion of the basic examination
techniques and findings, there is a perhaps
disproportionately long and in depth section
on airway problems, for these are often acute
and have to be managed immediately, without
leaving time to consult books, journals or even
colleagues first, so this area has to be studied
and understood in detail. Most of the other pa-
thology permits time to consult the textbooks
and refresh the memory. Otolaryngology, or
Otorhinolarynglogyheadandnecksurgery as
it has come to be known in many countries
includes not only the basic human commu-
nication apparatus of hearing and voice pro-
duction, and the upper air and food passages,
but has come to include a large proportion of
facial plastic surgery (looted from the plastic
surgeons) and neck surgery (from the general
surgeons) and base of skull surgery (from neu-
rosurgery—where they liked to approach this
area from the inside). This interspecialty piracy
is only justifiable if we can make a better job
of it, which often means concentrating on a
smaller area, and the whole field has begun to

see fragmentation and sub-specialisation again
in recent years.
     This book makes no attempt at encyclo-
paedic coverage of Otolaryngology, and many
areas are covered incompletely or not at all,
though I have tried to give an idea of the depth
and variety of the specialty. Should the reader
discover any obvious gaps, he should feel free to
complement the material from other sources.
     The student should always pass any new
material through his personal ‘filters’, to decide
what will be useful to him, and what on the oth-
er hand does not coincide with the knowledge
he has already acquired or even with common
sense. That material will need to be evaluated
in more detail.
     Much of the material has doubtlessly been
extracted over the years from a multitude of
sources, but it has been so successfully re-
worked by the subconscious memory that the
original works are all but unrecognisable. As
has been commented by James Hinton , phi-
losopher and first Otologist of Guy’s Hospital
London, “Nor do I profess to give accurately
the credit of their discoveries to each author,
nor even mention the source of each statement
made. Nothing is claimed as original” (in The
                                   The Basic ENT

Questions of Aural Surgery published in London
    The reader may take what he finds useful
and discard the rest.
    It is above all a practical approach to ENT
which should help the non-specialist to resolve
safely a good proportion of the problems he may
be faced with.

A Few Historical
     Historical aspects in science are not the
who and where and when (names, places and
dates) as it is usually taught in schools and
which successfully immunises the great ma-
jority of students against history for the rest of
their lives. Rather, we should look at the What
(what was thought, done, invented; what were
they looking for) and How (how did they think
of that, develop it, use it) and Why (why at that
time?, why him/her, why did the need arise)
     Otolaryngology as we practice it today is
a fairly recent specialty, dating only from the
end of the last century, when it was often as-
sociated with eye diseases, and surprisingly
sophisticated neck surgery. The different seg-
ments had been managed under a great variety
                                        The Basic ENT

of umbrellas, from the Embalmer-Surgeons of
Egypt (nasal and facial surgery is mentioned
in the Smith Papyrus which is over 2500 years
old), via the Toothpullers and Barber-Surgeons
of the middle ages, to the medically trained sur-
geons of the renaissance.
     Tagliacozzi carried out extensive nasal and
facial reconstruction in Bologna during the 17th
century, though many of his techniques had
been used by Hindu surgeons a thousand years
earlier, to reconstruct noses bitten off for adul-
tery. Ear pathology was little recognised, and
therefore not managed in much detail, (except
to remove wax and foreign bodies) until last cen-
tury when Joseph Toynbee made a systematic
study of the temporal bone pathology, followed
by Politzer who wrote one of the first major
textbooks on the ear, to convert into a serious
specialty what had until then been territory of
the “aurists”. Detailed Anatomical studies of
the ear had been carried out by Leonardo da
Vinci, Valsalva and ......., but little clinical man-
agement had resulted from those works.
     The invention of laryngeal mirror allowed
the throat and larynx to be incorporated nat-
urally into the a specialty which had made a
habit of peering into dark cavities. Electric light

helped tremendously to advance otology, laryn-
gology and rhinology, for flickering candle light
is not an optimal light source, and direct day-
light is inadequate, as it causes the examiner
to accommodate his eyes for daylight and not
for viewing small structures in dark cavities.
     From the turn of the century, French sur-
geons began to incorporate a large section of
head and neck surgery into Otolaryngology, and
turn of the century textbooks differ little from
modern ones.
     Eye problems were briefly included, but
quickly separated off again into ophthal-
     The major advancements in ENT this cen-
tury has been antibiotics and the operating
microscope. The former has allowed clinical
‘conservative’ management of previously sur-
gical problems, while the operating microscope
has brought delicate ear and larynx surgery,
previously restricted to the talented few, to
within the reach of all but the most clumsy
The Basic ENT

What do we need for a basic ENT

    The following list constitutes the minimum
requirements in equipment without which the
basic ENT examination and elemental treat-
ment becomes very difficult or remains incom-
plete. Obviously many more instruments are
routinely added to the basic set, but the ones
below are indispensable, though I have added
in brackets how a good number may be easily
adapted from readily available materials.

    •A light source — Head lamp (or head
                   mirror reflecting a strong
    •Diagnostic set with Otoscope
    •Tuning fork (musical tuning fork of
      440Hz used for tuning string instru-
                                The Basic ENT

   ments, is considerably cheaper than
   the ‘official’ ENT ones of 256 and 512Hz
   and work quite well—it also strikes a
   convenient compromise in the eternal
   discussion as to which is better, the
   256 or the 512Hz)
•Ear hook (a hair pin or a long lumbar
puncture needle with the end 2mm bent
   through 90º works well, but break the
   sharp tip off the needle first)
•Jobson-Horne probe (an orange stick
   can be wound with a small wisp of cot-
   ton and used to mop out an ear, rather
   then cotton buds or Q-tips which are
   too bulky)
•Nasal speculum (many different varieties
are available, most work fairly well)
•Bayonet / Tilley’s forceps (normal
non-toothed forceps may be used, but the
   hand holding them tends to obscure
   the narrow field of view into the nose or
•Tongue depressors (in the ENT sets used
 in Guy’s Hospital, they still have sev-
   eral large spoons with the handle bent
   through 90º, which make excellent
   tongue depressors. Bamboo may also
   be cut into adequate tongue depres-
•Laryngeal mirrors

(dental mirrors may be used on a longer
   handle, but make sure they are plane
   mirrors not the concave augmenting
   mirrors many dentists use, for they are
   impossible to focus on the larynx)
•Spirit lamp (an alcohol swab or small
cotton bud dipped in alcohol; even a
   disposable gas lighter may be used to
   warm the mirrors and prevent them
   getting fogged up by the patients
•Large IV catheter or needle 14-16 gauge
(for emergency cricothyroid puncture;
   the flexible canula mounted on a 20ml
   syringe is also useful for syringing ears
   and can be reused)
•Foley’s catheter 12,14 or 16
   (for posterior epistaxis)
•cotton wool / 1 inch gauze bandage /
Xylocaine spray/ ear drops / nasal
vasoconstrictor / AgNO3 (or
Trichloracetic acid) / syringe 20ml
•Suction — a motor or foot driven pump
(fine ear suction canulas can be made
   from lumbar puncture needles with the
   points filed off and bent through 30º,
   nasal canulas are usually available or
   can be improvised from nasogastric
                                The Basic ENT

(useful if available, but not essential—
  careful with ether anaesthetics)

       To study diseases of the ear, nose and
throat, it is necessary to learn and practice a
number of specialised techniques which allow
a more detailed examination and exploration of
these areas than is possible during a routine
medical examination. The normal must be
known well and studied before the pathological
will be recognised, so it is important to carry
out a complete ENT examination on all patients.
First we have to know what we are looking at
before we can know what we are looking for.

      The pinna and post auricular skin are
carefully examined for abnormalities, infections
or scars, and the pinna is then grasped gently
                                                 The Basic ENT

                        Pars flaccida

                                                    Lateral process of malle

                                           Manubrium of malleus

 Pars tensa

                                           Cone of light

between thumb and forefinger and pulled up-
wards and backwards (backwards and down-
wards in small children!) to straighten the
cartilagineous external auditory meatus, and
line it up with the bony meatus. A suitable
size otoscope is inserted (the otoscope is held
in the other hand like a pen, which facilitates
fine movements and avoids rough movements
likely to cause pain in the delicate meatal
structures) and a careful inspection is made of
the external meatus, and ear drum. Noting in
particular the position of the malleus handle
and the light reflex which points from the centre
of the drum down to the chin. A note is made
of any secretions; watery, mucoid, purulent,
bloodstained, odourless or foetid. Fluid bub-

bles visible behind the drum indicate fluid in
the middle ear, while changes in the vascular
patterns and consistency of the drum may be
due to inflammation or secretory otitis media.
    A small pneumatic bulb attached to the
otoscope is used to alternately increase and
decrease pressure in the external ear while
viewing the movements of the drum.
    Alternatively, the patient is asked to swal-
low while holding his nose closed (the Toynbee
Manoeuver) or clear his ears with his nose
closed (Valsalva Manoeuver) Both of these
cause pressure changes in the middle ear
which are observed through the otoscope as
movements of the drum.
    A small sketch is made of the eardrums,
indicating abnormalities, polyps, perforations
and secretions, for this not only obliges us to
examine with greater care, but to avoid the of-

    RightEar                  Left Ear
                                    The Basic ENT

ten gross inconsistencies found between written
descriptions. This way any future examiner will
know exactly what was seen.

b. TUNING FORK TESTS (Weber & Rinne)

       From the aspect of the ear and the pa-
tient’s history we may suspect a functional
problem with the hearing, which can be con-
firmed by a few simple tuning fork tests.
       Weber test: evaluates the difference be-
tween left and right ears by pressing the stem
of a vibrating tuning fork to the middle of the
patient’s forehead and asking him towards
which side the sound lateralises (in the normal
person it is either heard in both ears or in the
middle of the head). This test is very sensitive
and less than 10 dB difference between the
ears tends to be clearly lateralised towards one
side (test this on yourself by putting a finger
in one ear while holding the tuning fork to the
forehead; the sound immediately lateralises to
the blocked ear. The weber test tends to later-
alise towards the side of a conductive loss and
away from a sensory-neural loss. The patient
will have already indicated which ear is deaf,

so that if the sound is referred to the deaf
ear, we should suspect a conductive problem,
while if the sound lateralises to the good ear we
should suspect a sensory-neural hearing loss.
Remember though that we are only testing one
frequency and there may be more severe prob-
lems at other frequencies. The aspect of the
drum and middle ear should always be taken
into consideration.
        Rinne test: evaluates the difference be-
tween air and bone conduction in each ear, by
holding the prongs of the vibrating tuning fork
1 cm from the external ear until the patient
no longer hears the sound and then pressing
the stem against the mastoid area behind the
ear. If the patient still hears the sound, his
bone conduction is better than his air conduc-
tion (negative Rinne) and he therefore has a
conductive deafness. If he no longer hears the
sound (positive Rinne) he has either normal
hearing or a sensory deafness.
     If the examiner suspects a hearing loss, he
can compare the patients hearing with his own
(assuming he has normal hearing) by holding
the tuning fork in front of his own ear when the
patient no longer hears it. If he can still hear
it, he is less deaf than the patient, while if he
                                         The Basic ENT

cannot hear it they are at least equally deaf (this
is known as the Schwartz Test).
     A watch held a small distance from the ear
of the patient is also useful in comparing both
sides and obtaining a rough estimate of hear-
ing loss (most watches do not produce more
than 10dB)
     There are furthermore a good number of

            I                       II


specialised electronic instruments available
for testing the hearing. The most important
of which is the Pure Tone Audiometer which
tests a frequency range of 250 to 10,000 Hz
with intensities varying from 0 to 120 dB. Zero
Decibels (0dB) is softest sound a young person
can just hear in a very quiet room, while 120db
is the sound of a jet engine close by, so almost
the full range of the human ear can be explored
to discover the limits or threshold of hearing of
any particular patient. Furthermore, the bone
conduction thresholds are tested separately to
identify conductive and sensory hearing loss
with great accuracy. These results are then
plotted on a simple graph.


       The other function of the inner ear is
balance, as the vestibular labyrinth is one of
the most important components of equilibrium
system (with the eyes and the proprioceptive
nerve endings). The brainstem receives and
combines information from both labyrinths, the
optic tracts and the posterior columns of the
spinal cord, and integrates them into a sense
                                     The Basic ENT

of position in space, making the necessary pos-
tural adjustments to stop us falling over; with
the movements modulated and refined by the
cerebellum to prevent overcompensation
     Any alteration of the vestibular function ex-
presses itself as vertigo, usually rotational (the
patient feels that either he or the room is going
round in circles), and a careful clinical history
will go a long way to indicting the site and side
of the problem (a sensation or hallucination of
clockwise rotation implicates the right ear, while
anticlockwise rotation implicates the left ear).
     In the acute phase the patient generally
has horisontal nystagmus (first degree—only in
the direction of lateral gaze, second degree—on
looking straight ahead, and third degree even
when looking towards the opposite side). Be-
ware of a rotational or vertical nystagmus,
which is usually caused by a central lesion.
[Nystagmus is part of the normal oculo-ves-
tibular reflexes, which, whenever we move our
head, holds back the movements of the eyes for
a short time, before flicking them rapidly into a
new position, to prevent the visual fields blur-
ring on us every time we move our head, which
would be ecologically undesirable in dangerous
situations. When the head moves, the eyes

follow in a series of jerking movements while
keeping the visual fields focused. Try this by
focusing on the tip of your nose while moving
the head from side to side]
     A spontaneous nystagmus without the
head moving is an important indicator of ves-
tibular pathology.
     A latent or partially compensated nys-
tagmus may be demonstrated by taking the
patients head between the hands and rotating
it rapidly from side to side (as if shaking no,
which the patient will usually do anyway unless
the test is carefully explained to him first) This
is called the High Velocity VOR (vestibulo-oc-
ular-reflex) Test and is one of the most sensitive
and simplest of the vestibular tests.
     The basic neurological tests, well described
in the neurology text books are useful for dem-
onstrating or confirming falling tendency to one
     The only test which examines both laby-
rinths independently is the Caloric Test, which
in its most basic form consists of injection 1
ml of ice water into the external ear canal and
measuring the duration of the nystagmus which
this procedure induces (towards the opposite
ear). Explain the test carefully to the patient
                                     The Basic ENT

beforehand, emphasising that he may feel dizzy
for a minute or so, and do not use more than 1
ml or the patient may vomit all over your clean
white coat.
     After 5 minutes the test is repeated on the
opposite ear.
     Try observing vessels of the optic fundi
with the ophthalmoscope to identify a faint
nystagmus or help determine the end point of
a self-limiting nystagmus.
     A slightly more sophisticated version of the
caloric test (described by Hallpike) requires the
infusion of first warm and then cool water (ex-
actly 8ºC above and below body temperature)
into the ear for one minute and then registering
the duration of the nystagmus (the mnemonic
COWS indicates the expected direction of the
normal response—Cold Opposite Warm Same)
and the results are drawn on a simple graph to
compare the two sides.


      The nose is inspected laterally and
straight on to detect anatomical deviations and

skin abnormalities.
     Then, using a head lamp mirror or oto-
scope, the tip of the nose is lifted to inspect the
vestibule. In children this is sufficient to allow
a view of the internal nose, and it is usually
unnecessary to use a nasal speculum which
tends to frighten them. In adults the nasal
speculum (or large otoscope cone) is inserted
to inspect the inside of the nose, noting the
colour of the mucosa, condition of the inferior
and middle turbinates, deviations of the septum
and crusting, secretions or bleeding. A small
amount of vasoconstrictor and local anaesthetic
is then applied to the nose as drops, spray or
on a cotton pledget and left for 5 minutes, to
decongest the nose and make subsequent ex-
ploration painless.
     Review the nasal septum on both sides to
note deviations, prominent vessels and bleed-
ing. Check the inferior and middle turbinates
(these are vascular swellings projecting into the
lumen from the side, to control airflow through
the nose; there is also a superior turbinate but
it is difficult to see) The turbinates are often
confused with polyps, but attempts to remove
them causes severe pain and profuse bleeding
                                                  The Basic ENT



                                         NASAL OBSTRUCTION


differentiate the two by touching gently with
some forceps, as polyps are softer, paler and
insensitive, while turbinates are firmer and
very sensitive to pain. With a little experience
they are easily distinguished by aspect alone.
Assess the condition of the mucosa; pale, hy-
peraemic, atrophic etc., and the nasal secre-
tions; transparent, mucopurulent (yellowish of
even greenish), bloodstained. A small mirror
may be used to allow the patient to see into his
own nose as we are examining it. In children
the same mirror held under the nose shows by

misting up if both nostrils are patent incase of
a suspected choanal atresia. Any abnormal
growths, ulcers, polyps should be noted. As in
the ear, a standard sketch is useful for indi-
cating any abnormalities.


Use two tongue depressors (one in each hand)
to examine the oral cavity systematically:

    •Upper buccal sulcus, cheek mucosa and
      parotid duct openings (opposite upper
      second molar)
    •Lower buccal sulcus and mucosa
    •Teeth and alveolar margins
    •Retromolar trigones
    •Hard and soft palates, including soft
      palate mobility and symmetry.
    •Tongue, dorsum and base
    •Floor of mouth and submandibular
    •Anterior tonsillar pillars
    •Posterior wall of oropharynx

   Any visible lesions should be palpated bi-
                                     The Basic ENT


       This examination should always be car-
ried out with the confidence of vast experience,
even the first times, or the patient becomes
tense and does not relax sufficiently to allow a
view of the larynx.
    With the patient sitting back in his chair,
gently draw his head forward to position the
head in extension on a slightly flexed neck
(the taco eating position). Ask him to open his
mouth and stick out his tongue which you grasp
(gently) with a gauze swab (not cotton wool or
Kleenex please or an unhappy patient will be
spitting fuzz for an hour after the procedure).
The mirror is warmed over a spirit lamp or in
hot water and tested against the palm of your
hand (most books indicate the back of the hand,
but of it is too hot it will make you jump and
few patients will allow you to put the mirror into
their throat after that). A little soap rubbed on
the mirror also prevents fogging.
    Insert the mirror carefully into the mouth,
taking care not to clink it against the teeth on
the way (which also makes the patient nervous)

and gently press it against the soft palate and
uvula, pushing the palate up with the mirror
until a view of the epiglottis is obtained. Light
from a headlight or forehead mirror is directed
onto the laryngeal mirror to illuminate the lar-
ynx. The patient who all the while is breathing
through the mouth, is then asked to say a long
Eeeee, which lifts up the larynx, folds back the
epiglottis (forward actually but the mirror in-
verts everything) and with a bit of luck reveals
the vocal cords underneath. This takes practice
and patience. In a difficult examination, a little
Xylocaine spray may be applied to the throat
but it is generally not as helpful as developing
the stance of a confident examiner who seems
to know what he is doing.
     The following structures are examine sys-
tematically to avoid missing any and having to
go back for a second look later:
     • Base of tongue (there is usually some
irregular lymphoid tissue here, part of the ring
of Waldeyer which should not be confused with
tumour mass)
     • Epiglottis (the little Fig leaf which covers
the modesty of the vocal cords and sometimes
refuses to let us see them)
     • Valleculae (those little cavities on either
                                      The Basic ENT

side of the epiglottis)
     • Vocal Cords (the true vocal cords are like
two little white ribbons attached to the epiglottis
anteriorly—looks posterior due to mirror inver-
sion— and to the arytenoid further back)
     • False cords (fleshy margins slightly above
and lateral to the true cords and occasionally
confused with them)
     • Anterior commissure (where the vocal
cords join the epiglottis)
     • Posterior commissure (between the
arytenoid cartilages; separating the larynx
from the hypopharynx above the oesophagus
entry—again, this looks anterior on the mirror
but a review of the anatomy soon reveals the
     • Arytenoids (small humps of cartilage to
which the vocal cords attach on one side and
the laryngeal muscles on the other—that is how
the cords can move)
     • Often the first tracheal rings and tracheal
mucosa are visible below the vocal cords.
     The patient is asked then to breathe deeply
to asses the mobility of the cords (which open
on breathing and close on phonating!)
     Examine carefully the edges of the vocal
cords, for a patient who is hoarse usually has
                                     The Basic ENT

a problem with the mobility or the structure
of the vocal cords. Even a small nodule or a
slight inflammation may affect the clarity of
the voice.
     Again, use a sketch to show abnormalities.
With a little practice beforehand, even the worst
artist is capable of making an intelligible line
drawing of the larynx.


       The nasopharynx can also be examined
in a similar way to the larynx, except a smaller
mirror is normally used, and the tongue in-
stead of being stuck out and grasped with a
gauze, is depressed with a tongue depressor
to provide sufficient space between the base of
the tongue and the uvula, to pass the mirror
(directed upwards this time), and examine the
     First identify the posterior end of the nasal
septum, a thin vertical band separating the
round openings of the posterior choanas where
the posterior ends of the inferior turbinates are
usually just visible. Inferiorly you can see the
adenoidal tissue; similar in appearance to the

lymphoid tissue of the tongue base, while on
either side there are the Eustachian tube open-
ings, surrounded by the slightly raise dough-
nuts of the eustachian cushions. Above these
are the areas called the fossae of Rosenmüller,
notorious for the formation of nasopharyngeal
cancer. (use a sketch)


      The examination of the neck must be
carried out systematically, so that no area is
missed. Standing behind the seated patient,
and running the fingers from the submental
area back along the angle of the jaw, palpating
successively for: submental lymph nodes,
submandibular lymph nodes, submandibular
salivary gland, parotid gland (including the
deep lobe between the angle of the jaw and the
mastoid—do not mistake the lateral process of
the atlas for a parotid tumour), pre and post
auricular nodes, occipital lymph nodes. The
anterior borders of the sternomastoid mus-
cles are palpated down to the clavicles, from
where the supraclavicular areas are examined
backwards to the anterior border of the tra-
                                       The Basic ENT

pezius (enlarged nodes found in this area are
usually due to a lung of stomach cancer). The
fingers are then run over the posterior triangle
(between the anterior border of the trapezius
and the posterior border of the sternomastoid,
and the deep jugular nodes are palpated by
encircling the sternomastoid muscles between
thumb and forefinger and running the fingers
down from mastoid to sternum. Then, standing
in front of the patient, the larynx is palpated for
mobility and crepitus, and the thyroid gland
is examined along the sides of the larynx and
trachea (it is difficult to palpate unless enlarged,
and finally the trachea is located down to the
sternal notch (it should be in the midline un-
less something is pushing it to one side). Any
abnormal cysts, tumours, fistulas, lymph nodes
etc. are carefully located on a simple sketch of
the neck. Any tumour or lymph node which
persist after antibiotic treatment should be as-
pirated for cytology (see relevant chapter).


        A concise examination of the cranial
nerves is part of the ENT examination, espe-
cially in patients with vertigo or other neurologi-
cal symptoms. If organised efficiently it need
not take more than 5 to 10 minutes, especially
since much of the area has already been exam-
ined in the basic ENT examination commented

      I - Olfactory nerve. The history should
give indications of olfactory alterations, and
anosmia (complete loss of the sense of smell)
is distinguished from hyposmia by asking the
patient if he tastes his food. Since except for
the basic taste modalities of salt, sweet, bitter
and sour, all other “taste” is due to the sense
of smell, via the postnasal spaces. Hyposmia
tends to not affect the taste of food, while in
anosmia the patient complains bitterly of in-
sipid and tasteless food (and rightly so, for one
of life’s most lasting pleasures has been taken
away from him). Confirm anosmia by having
the patient close his eyes and placing some
common household substances under his nose;
ground coffee, spices (not pepper which stimu-
                                     The Basic ENT

lates the Trigeminal nerve) perfume etc., while
asking him to identify them. Generally if he can
smell one, he can smell them all, so complicated
smell testing kits are unnecessary.
    Anosmia is usually due to damage of the
olfactory nerves by virus or trauma, but a tu-
mour must be ruled out, especially in the rare
unilateral anosmia. Hyposmia is often due to
nasal obstruction or sinusitis and often cur-

     II - Optic nerve. Explore the patients vis-
ual fields by sitting in front of him and asking
him to look at your nose while moving your
hands gradually in from arms length until he
identifies your fingers. Visual fields of examiner
and patient should roughly coincide. This is
followed by fundoscopy and review of pupillary
reactions to light and accommodation. Visual
Acuity is checked for each eye with Snellen’s
letter chart

    III, IV, VI - Oculomotor, Trochlear and
Abducent nerves.
    These nerves all move the eyes and are
quickly tested by asking the patient to follow
the examiners finger in the different direction,

while observing for signs of paralysis and asking
the patient to report double vision. Paralysis of
the Abducent nerve (VI) - which innervates the
Lateral Rectus muscle, prevents the eye from
abducting (it seems to get stuck in the midline
when the patient looks towards the affected
side, and he will indicate double vision when
he looks towards that side.
    Paralysis of the Trochlear nerve (IV) which
innervates the Superior Oblique muscle, is the
most subtle, to spot, and the patient indicates
double vision on looking down (especially awk-
ward for going down stairs).
    The Oculomotor nerve (III) controls all the
other eye muscles and paralysis is easy to

    V - Trigeminal nerve. This is the large
sensory nerve to the greater part of the face;
inside and out, whose three major branches
are the Ophthalmic, the Maxillary and the
Mandibular divisions. These are tested with a
pledget of cotton wool on the sides of the face,
and by the corneal reflex, which causes the pa-
tient to blink if we brush the cornea edge with
a strand from the cotton wool.
                                      The Basic ENT

     VII- Facial nerve. This nerve is automati-
cally assessed as we take the patients history,
but look for asymmetry, asking the patient to
show his teeth and close his eyes tightly. Look
for Bell’s sign of peripheral facial palsy (turning
up of the eye seen through incompletely closed
eyelids. In case of paralysis we may try to locate
the level of the injury with a few simple tests and
a thorough understanding of the anatomy. In-
nervation of the lacrimal glands separates from
the facial nerve at the genicular ganglion, so
that injury below that level will not interfere
with the tear production. This is tested with a
small strip of litmus or filter paper draped from
each lower eyelids for a few minutes and com-
paring the length to which they become soaked
with tears. A marked difference on the affected
side may indicate facial nerve injury above the
ganglion(known a Schrimer’s Test) The chorda
tympani separates off from the facial nerve in
the mastoid and curves back up through the
middle ear to join the Lingual nerve and supply
taste to the anterior 2/3 of the tongue on the
same side, so that carefully comparing taste
on both sides of the tongue we can distinguish
a lesion above the descending mastoid portion
of the facial nerve (The chorda tympani itself

may also be affected by an inflammatory proc-
ess in the middle ear or by surgery). Then, as
it emerges from the mastoid foramen, the nerve
quickly splits up into its 4 or 5 main branches
towards, forehead and eye, midface, mouth, and
single branch injuries indicate a lesion in the
face or parotid region.

    VIII - Vestibulo-Acoustic nerve. We have
already examined this nerve with the tuning
fork and vestibular tests described above.

    IX, X, XI - Glossopharyngeal, Vagus and
Accessory nerves. These are examined to-
gether during the oropharyngeal examination
and indirect laryngoscopy. A normal gag reflex
and normal vocal cord movements generally in-
dicate that these nerves are intact. Conversely,
any detected abnormality in vocal cord move-
ment, palatal elevation or sensitivity of the
oropharynx, must be individually assessed to
determine cause and level of the lesion. The
innervation of the trapezius and sternomastoid
muscles from the spinal part of the accessory
nerve is quickly checked by asking the patient
to shrug his shoulders, and rotate his head
against resistance of the examiner’s hand.
                                    The Basic ENT

    XII - Hypoglossal nerve. Tongue move-
ments, asymmetry or fasciculations have also
already been observed during the oral exami-

     Coordination, Balance and the higher cer-
ebral functions are roughly assessed during
the examination and History. Suspicion of
abnormality requires a full formal neurologi-
cal examination.

     Once we have mastered the basic exami-
nation techniques it is necessary to know how
to deal with the emergencies and common prob-
lems. For the emergencies, treatment must
be instituted quickly to prevent permanent
disability and loss of function. There is often
no time to consult a specialist, so it is impor-
tant to know how to deal with these problems
quickly and efficiently. Usually the circum-
stances and equipment are not optimal either,
so it may be necessary to improvise. But as
in all surgical problems , if you have studied
and thought about the possible complications
of any procedure and examined the solutions to
these problems beforehand, it is easier under

the stress of an emergency, to follow an already
existent trail of thought rather than to have to
break new ground. Admittedly, some surgeons
work best under stress and develop very crea-
tive solutions, but these surgeons are a rare
breed, and for most of us it is better that we
have at least some notion of what we ought to
be doing. Praeceptorum Optimum was the motto
of Gaspare Tagliacozzi one of the founders of
plastic surgery several centuries ago, when the
penalties for surgical complications were severe
(for the patient and for the surgeon).


     Use a 10 or 20 ml syringe with an 18 gauge
(green) needle, a few microscope slides and a
jar of alcohol, or a can of clear hair spray.
     1. At the start of the procedure, fill the
syringe half way with air. This not only makes
it easier to wrap the small fingers around the
plunger and pull a vacuum with one hand, but
also facilitates the expulsion of the aspirated
material in the needle onto the slide.
     2. Locate the nodule or tumour, and fix it
                                     The Basic ENT

between the thumb and index finger of the left
      3. Insert the needle through the skin into
the centre of the nodule, and pull the plunger
of the syringe out as far as possible without
separating it from the syringe.
      4. With the plunger held out, slightly re-
tract the needle from the nodule and insert
it again at another angle, repeating this ma-
noeuvre several times.
      5. Slowly remove the vacuum by letting
the plunger attain its original position (half way
down the syringe)
      6. Remove the syringe.
      7. express the aspirated material from the
needle onto a microscope slide and cover it with
a second slide to squash the material between
the two. Quickly insert both slides into a small
jar of alcohol so that the cellular material is
covered, or spray them with some clear hair
spray. Make 2 more slides with any material
left in the syringe.
      8. Take the jar with alcohol and slides to
the pathologist / cytologist with as much clinical
information as possible for the cells are some-
times difficult to interpret. Or roll the slides
fixed with hairspray in a sheet of clean paper so

that they do not stick together, and post them
to the nearest reliable laboratory with a cover-
ing letter explaining the clinical detail.

     With a little experience it is not difficult
to see (macroscopically) if the cellular mate-
rial is sufficient, and avoid the cytology report
coming back “insufficient material” Too much
blood aspirate tends to produce inadequate
results and the puncture should be repeated.
Malignant tumours have looser stroma and is
thus easier to aspirate, while lipomas and other
benign tumours are often more difficult to as-
pirate. If the material looks insufficient repeat
the puncture.
                                The Basic ENT

 I have made a selection of ENT emergencies
and common problems, and how they may be

       Airway problems are the most acute of
medical emergencies, for lack of air leads to un-
consciousness in 5 minutes and brain damage
in 10, so there is often little time to act and less
time to call for help. Every physician should
know how to adequately diagnose and initiate
treatment of these problems.
     The first difficulty is to locate the site of the
obstruction; is it supraglottic, is the obstruction
at the larynx, or in the trachea? in the bronchi?
or further down the lungs. Is it back-pressure
from a failing heart which is filling up the lungs
with fluid? or perhaps a collapsed lung from a
pneumothorax? or is it asthma? Since there is
usually no time to go to the library and research
this problem it is worth spending a little time
                                     The Basic ENT

in examining the causes.
       Due to the potentially life threatening
nature of an upper respiratory tract obstruc-
tion, a diagnosis must be made quickly and
accurately on the basis of scant physical signs
and an often inadequate history. The clinical
atmosphere is almost invariably tense and the
examining physicians’ skills are taxed to the
limit. There is virtually no room for error, and
speed is essential if tragedy is to be avoided.
This is one of the few real emergency situations
in otolaryngology and medicine.
       The patient should be approached in a
systematic fashion. A history is taken rapidly
wherever possible, with emphasis on duration,
onset and progression. Inquiring about pre-
vious intubation and foreign body aspiration.
Careful attention is paid to the patients voice
at this point, for clues about vocal cord palsies
or supraglottic swelling (hot potato voice).
       Examination includes nasal and oral
airways (without instrumentation), neck and
chest. Looking for retractions, tachypnea, nasal
flaring and cyanosis. Remember to check the
mandible and tongue in case of trauma.
       Auscultation follows; the typical stridor
of airway obstruction is usually clearly audible,

being caused by turbulent airflow through a
narrowed airway. But the neck and chest
should be carefully examined with a stetho-
scope for crepitations, stridor and the respi-
ratory cycle (normally inspiration is faster than
       Then the neck and chest are palpated
with great care: Floor of mouth and neck for
tumours and swellings, trachea and larynx for
deviations and crepitations.
       If available a fibre-optic endoscope may
be passed transnasally to assess the larynx, but
tongue depressors and laryngeal mirrors are
avoided until epiglottitis has been ruled out.
       Radiology if available, should consist ini-
tially of plain A-P and lateral neck and chest
     Further studies may include blood gasses
and pulmonary function tests.

     Ideally the patient is accompanied by a
doctor at all times until a diagnosis is made,
and there should be a tracheotomy set within
easy reach in case the obstruction progresses
to respiratory failure.

      If a firm diagnosis has not been made
                                     The Basic ENT

at this point, a fibreoptic or rigid endoscopy
may be carried out in the operating room, with
a basic surgical team available and prepared to
proceed immediately to intubation or tracheo-
tomy if there is further airway compromise.
       The first step is to accurately locate the
level of obstruction, and for diagnostic pur-
poses, the upper respiratory tract may be con-
veniently subdivided into:


         - SUPRA-GLOTTIS
         - GLOTTIS
         - INFRA-GLOTTIS

         - CERVICAL
         - THORACIC

   Obstruction may occur at any level, and
symptoms vary subtly with the localisation.

      Stridor is the cardinal symptom of up-

per respiratory tract obstruction. Caused
by turbulent airflow in a narrowed airway, it
may be either inspiratory, expiratory, or both;
depending on the location of the obstruction.
Careful consideration of this symptom allows
us to localise the pathology, even in the absence
of other diagnostic aides.
     Supraglottic and supra-laryngeal tissues
are loosely supported and tend to collapse in-
ward on inspiration, so that obstruction tends
to cause inspiratory stridor
     Pathology at glottic, subglottic and cervical
tracheal level causes both expiratory and in-
spiratory stridor (biphasic stridor). The tis-
sues have firm cartilage support and are less
susceptible to the Venturi effect, so that the air
flow depends on absolute lumen size.
     The intrathoracic trachea is less well sup-
ported by cartilage, and positive pressure of
the chest wall contraction combined with the
Venturi effect causes expiratory stridor.
                                    The Basic ENT




       The possible causes of upper airway ob-
struction are manifold and may be subdivided
as all pathology into:


in the categories Supralaryngeal, Supraglottic,
Glottic, Subglottic and Tracheal. Since the list
is very extensive, only the most important ex-
amples will be mentioned here:


      Congenital: Choanal atresia
                  Cleft palate

      Inflammatory: Ludwig’s angina
                    Retropharyngeal abscess

      Traumatic: Facial trauma
                 Burns (chemical/physical)
                 Postoperative swelling

      Immunologic: Allergic oedema

      Neoplastic: Lingual/pharyngeal

      Miscellaneous: OSAS

     In bilateral Choanal atresia , a membra-
nous and/or bony septum closes off the pos-
terior choana where the nasal cavities join to
form the nasopharynx (above the soft palate),
must be diagnosed at birth. Since the neonate
does not possess well developed mouth breath-
                                     The Basic ENT

ing reflexes, it will attempt to breathe through
the nose until almost cyanotic. Tonsillar
hypertrophy is rarely cause for severe airway
obstruction, but it may lead to obstructive sleep
apnoea. In severe facial trauma with man-
dibular and/or maxillary fractures, an airway
should be secured as soon as possible, since
slight oedema or displacement of the fractures
may cause obstruction. Neoplasms must be
large before they compromise the airway at this
level. Obstructive sleep apnoea syndrome
should be mentioned here as an intermittent
acute upper respiratory tract obstruction dur-
ing REM sleep. During this sleep stage, the
palatal, lingual and pharyngeal tissues relax
sufficiently to cause complete obstruction of
an already compromised airway. This leads to
awakening reflexes which interrupt the REM
stage and increase muscle tone sufficiently to
allow breathing to proceed. The consequences
of these frequent (partial) awakenings and re-
duced REM sleep is not of concern here, but
the apnoeic episode causes a severe drop in
oxygen saturation and an increase in carbon
dioxide levels. Many of the causes mentioned
above may precipitate the syndrome.


      Congenital: Atresia and webs

      Inflammatory: Epiglottitis

      Traumatic: Neck trauma
                 Surgical oedema

      Immunologic: Allergies
                   Angioneurotic oedema?

      Neoplastic: Carcinoma

     Of the congenital abnormalities, most
are evident at birth, though laryngomalacia
(abnormal flacidity of the laryngeal cartilages,
which get sucked inwards during inspiration,
causing stridor), may not cause symptoms for
some weeks postpartum. The stridor is usu-
ally not severe enough to require treatment,
but condition needs to be carefully explained to
                                     The Basic ENT

the parents, as it may be several years before
the cartilagineous structures are sufficiently
mature to fully support the airway, and care
should be taken during upper respiratory in-
fections which may further compromise the
     Epiglottitis is an inflammation of the
epiglottis and supraglottic structures; usu-
ally associated with a Haemophilus Influenza
infection, and characterised by a ‘hot potato’
voice and the ‘rising sun’ sign (with the mouth
fully open and tongue extended, the bright red
swollen epiglottis is seen rising above the base
of the tongue) especially in young children. The
use of tongue depressors and laryngeal mirrors
may lead to acute obstruction and is strictly
discouraged. There is a significant mortality
reported for epiglottitis, and the patient must
be closely observed at all time. A tracheotomy
is carried out if the stridor seems to be progres-
sive. Allergic and angioneurotic oedema may
lead to rapidly progressing but rarely complete
obstruction. Granulomatous diseases such as
tuberculosis and respiratory scleroma may
lead to severe fibrosis and stenosis of the up-
per airway. Though this is a chronic process,
any secondary infection in the narrowed airway

induces stridor. A similar condition occurs with
tumours of the upper airway, which explains
the temporary improvement with antibiotic and
steroid treatment.


      Congenital: Webs and atresia

                 Intubation oedema

      Traumatic: Laryngeal fracture
                 Foreign body

      Immunologic: Granulomas

      Neoplastic: Benign and malignant
                  carcinoma / lymphoma /
                  sarcoma / papilloma /
                  haemangioma etc.
                                     The Basic ENT

      Neurologic: Vocal cord paralysis

     The glottis is a mobile structure within this
rigid part of the upper airway, which gives it
some unique properties. It’s function is not as
is so often thought for voice production, but
as a protection for the lungs; voice production
is a purely coincidental side effect! As it is the
generator of the voice however, pathology at
this level is generally reflected as hoarseness
long before stridor occurs (with exception of bi-
lateral vocal cord paralysis in adduction, which
causes severe stridor with little voice changes)
Complete webs and atresia are usually in-
compatible with life, unless diagnosed and
treated immediately at birth. Partial atresia
manifest as feeding difficulties with or without
aspiration in the first few weeks of life. Inflam-
matory upper respiratory tract problems are
common, and cause stridor earlier in infants,
due to the relatively narrower airway. Patients
with trauma to the larynx (not uncommon in
football, karate and traffic accidents) should
be carefully observed, as oedema may cause
respiratory insufficiency in a matter of hours.

Foreign bodies frequently become lodged at
glottic level, where the upper airway is nar-
rowest and protective laryngeal spasm prevents
them from passing further down. Subsequent
cough reflex normally propels the object out of
the airway. If not , the laryngeal spasm persists
until hypoxia overrides and the patient inhales
forcefully, allowing the object to reach the ca-
rina of bronchi, with serious consequences. The
protective mechanisms only rarely fail.
     Granulomatous processes from tuber-
culosis or (occasionally) prolonged intubation
cause stridor from inflammation initially and
later from fibrosis. Early treatment is manda-
tory, for surgical treatment of a stenosed glottis
is unsatisfactory in the best hands, due to the
difficulty in restoring the dynamic functioning
of the larynx. Laryngeal tuberculosis is one of
the few situations in which the use of corticos-
teroids is justified with an infective process,
to try and prevent fibrosis. Neoplasms at vo-
cal cord level present early on with dysphonia
(hoarseness), and early treatment is even more
important than in tuberculosis. Any patient
(especially a smoker) complaining of persistent
hoarseness for more than 6 weeks requires a
firm diagnosis as soon as possible, preferably
                                     The Basic ENT

with biopsy of any lesions found on the vocal
cords. In the paediatric age group, laryngeal
papilloma is the most common tumour. Of viral
origin, and often associated with condyloma in
the mother, they present little diagnostic diffi-
culty, but a serious therapeutic problem. Often
requiring multiple surgeries, the papilloma are
best removed early, before the laryngeal anat-
omy becomes distorted and the risk of perma-
nent scarring is higher. Tracheotomy must
be avoided, since bronchial seeding is more
common following this procedure. Unilateral
vocal cord paralysis causes dysphonia, but
usually does not cause stridor except during
effort. Bilateral palsy produces no hoarseness
(the cords are adducted in the midline), but
causes almost immediate severe stridor and
usually requires a tracheotomy. A vocal cord
paralysis must be fully investigated, not only at
glottic level, but along the entire course of the
recurrent and vagus nerves, to identify the site
of the lesion. Apart from thyroid surgery, the
most common causes of left Recurrent nerve
paralysis are cardiac and pulmonary pathology;
tuberculosis, neoplasms, aorta aneurysm etc.


    Congenital: Stenosis

    Inflammatory: Laryngo-tracheo-bronchitis

      Traumatic: Foreign body
                 Post-intubation stenosis
                 Post-tracheotomy stenosis

      Immunological:Granuloma tuberculosis
                    /scleroma/ intubation

      Neoplastic: Tumours

     Laryngo-tracheo-bronchitis (Croup) is a
viral inflammation of the upper airways. In 10-
15% there is an associated bacterial infection
with H.Influenza which will require antibiotic
treatment. There is considerable controversy
surrounding the use of antibiotics for this condi-
tion, but in view of the potentially life threatening
consequences, and the difficulty in obtaining ac-
curate cultures from the affected areas, I con-
                                     The Basic ENT

sider that 10-15% is sufficiently high to justify
antibiotic use in all cases. Foreign bodies do
not tend to lodge in the subglottic or tracheal
regions, for having passed the glottis they drop
straight down to the carina or main bronchi (in
adults most often the right, in children under
3 predominantly the left)
     Post intubation stenosis develops at the
level of the endotracheal tube cuff (subglot-
tis) during the first weeks after a prolonged
intubation. Excessive cuff pressure causes
necrosis of the tracheal mucosa, and the ex-
posed tracheal cartilages become infected and
degenerate or liquefy, leaving a weak zone in
the trachea which gradually stenoses after extu-
bation. Clinically, there is progressive stridor
due to a combination of the Venturi effect on
the unsupported (by cartilagineous rings) seg-
ment, and progressive stenosis of the tracheal
lumen. Post tracheotomy stenosis is often
due to resection of a tracheal window, which
some authors recommend, but may result from
infection of the exposed cartilages. It generally
leads to a narrow stenotic site than the longer
intubation stenosis and is simpler to resect in
end-to-end anastomosis during tracheoplasty,
which is the treatment of choice for tracheal

stenosis (dilatation with oesophageal dilators
or a Foleys catheter inflated at the stenotic
site should be attempted first, but are often

       Upper airway obstruction may be pro-
duced by pathology outside the respiratory
tract. Thyroid tumours may cause stridor
by displacing the larynx and trachea, or by
infiltrating these structures (especially med-
ullary carcinoma). Similarly , mediastinal or
pulmonary tumours or metastases compress
or displace the trachea. In children, a foreign
body in the oesophagus or a congenital vascular
anomaly may compress the airway sufficiently
to cause obstruction. Deep neck abscesses
may also compromise the airway.

    In any patient with airway obstruction
therefore, the cause and localisation must be
quickly and systematically searched for so that
adequate therapy may be instituted.
                                     The Basic ENT


     We need to establish an adequate airway. It
is usually best to go from less invasive to more
invasive with surgical therapy.
     An oral airway may be all that is required,
in an unconscious patient or one with maxil-
lofacial trauma, and should certainly be tried
first. The next step is clearing out blood or se-
cretions from the throat, and if the patient does
not breathe better, we progress to an intubation
if possible (take great care in cervical trauma)
An anaesthetic laryngoscope is inserted over the
base of tongue up to the valleculae and used to
lever the tongue and epiglottis forward to obtain
a view of the vocal cords. An adequate sized en-
dotracheal tube is inserted through the cords
and connected to an Ambu bag or anaesthetic
machine. Listen carefully to the breath sounds
and check the chest expansion—oesophageal
intubation is a frequent error, and the stomach
is not an optimal organ for oxygen exchange .
     If there is no laryngoscope available (or it
has no batteries), an attempt may be made with

a suitable head lamp, but it is usually necessary
to progress to Cricothyroid membrane puncture
or tracheotomy. An exception may be made in
small children, where a tracheotomy is more
hazardous for various reasons we shall see be-
low, and the neck is short enough to reach the
larynx with the index finger. Blind intubation
may be attempted by inserting one finger into
the oesophagus while palpating the arytenoid
cartilages anteriorly, and riding the endotra-
cheal tube over the finger into the larynx and
trachea. This however should not be attempted
without having a tracheotomy set ready, for if
the attempt fails the stimulation of the larynx
frequently leads to laryngeal spasm and com-
plete airway obstruction.
     The next step is a cricothyroid (membrane)
puncture, which in inexperienced hands is
probably the safest procedure. Gently palpate
the laryngeal cartilages laterally and move the
fingers to the midline at the Adam’s apple. Pal-
pating downwards you will encounter another
cartilagineous bump which is the cricoid carti-
lage (try this) between the two is an excavation
closed by the cricothyroid membrane. Insert the
biggest needle you can find (14 gauge is best
or several smaller needles) through this mem-
                                    The Basic ENT

brane, angling it downwards. If you are in the
trachea, air will immediately rush in. Connect
up to 100% oxygen if available. This is a tem-
porary measure, but will buy you time to get
the patient to operating room and resolve his
airway obstruction.
    The final resort is a tracheotomy, and no
matter what you may see in the movies, this is
not a procedure that can be carried out with a
pen knife and ballpoint pen at home or in the
street or even at the patients bedside, unless
you have extensive experience in head and neck
surgery. [You only have to imagine the worst
case scenario where you are not successful and
the police arrive to find you standing over the
body with a bloodied swiss army knife in your
    It is a surgical procedure which requires
adequate lighting and instruments, anatomical
knowledge and surgical experience if it is to be
carried out without complications.

EMERGENCY Tracheotomy.

    This procedure is carried out under local

     The patient is placed on his back, with the
neck extended. The thyroid and cricoid carti-
lages are palpated, and the skin is infiltrated
for a horizontal incision of 6-7cm at the cricoid
level. The subcutaneous tissues are infiltrated
and lastly the needle is passed into the tra-
cheal lumen (aspirate a little air to confirm its
position) so that 1-2ml of Lignocaine can be
infiltrated into the tracheal lumen. This accu-
rately locates the trachea and also suppresses
the cough reflex which tends to spray the sur-
gical team with blood as soon as the trachea is
opened. The horizontal incision passes cleanly
through the skin and platysma whereafter the
blunt dissection continues in the vertical plane
between the infra hyoid strap muscles to locate
the tracheal and cricoid cartilages — these are
easily palpated. The front of the trachea is cov-
ered then only by the thyroid isthmus which
must be handled with care as it tends to bleed
profusely. The isthmus is separated off the
trachea with artery forceps or dissecting scis-
sors (in a caudal direction to avoid dissecting
up under the cricoid) and clamped between two
artery forceps before being cut and ligated. In
an emergency the isthmus can be pushed
                                     The Basic ENT

down or up to provide access to the 2nd and
3rd cartilages, but pressure erosion against
the tracheotomy tube may cause unexpected
postoperative bleeding, so it is safer to section
it. The important point is to stay in the midline
and palpate the trachea when in doubt. (spe-
cial care must be taken with Thyroid tumours
which may push the trachea laterally and I
have seen the dissection carried down into the
carotid artery with fatal results)
     There are several methods described for
opening the trachea but the safest is cutting
vertically through the 2nd and 3rd tracheal
cartilages in the midline. (a horizontal inci-
sion between the cartilages gives less stenosis
when the tracheotomy heals, but it is more
difficult to insert the tube, and easier to injure
the recurrent nerves as they pass upwards on
either side in the sulcus between the trachea
and oesophagus) As soon as the trachea is
opened the patient takes a deep breath—re-
member he is awake—, so clean the blood from
around the trachea before opening, to prevent
aspiration. Separate the tracheal incision with
some hooks, and insert the tracheotomy tube,
or endotracheal tube, or any other available
tube. The skin incision is roughly closed by

one suture on either side of the tube (a hermetic
seal will result in postoperative subcutaneous
emphysema) and no drain is necessary since
the tube doubles as wound drain. In children
take special care of the Innominate artery which
rises above the sternum on neck extension
and may be injured during the dissection —it
bleeds!! and is very difficult to repair. The risk
of postoperative extubation in children is such
that it is wise to put a 2-0 reference suture on
either side of the trachea which can be taped to
the neck and removed after 5 days. No attempt
should be made to change the tracheotomy tube
within the first week of operation, as the tract
has not yet adequately formed and reposition
of the tube is awkward to impossible. A work
around to this problem is to insert a small
calibre feeding or nasogastric tube into the
tracheotomy tube to be removed and removing
the tube while leaving the nasogastric tube in
its place. The new tracheotomy tube is then
more easily inserted over the nasogastric tube
before the latter is withdrawn.
                               The Basic ENT

Fig. 1

     Fig. 2





     Fig. 3

                      Fig. 4


       Slight bleeding from the nose or gums
is an everyday occurrence which usually does
not worry the patient, similarly, tuberculous
patients often have a little blood mixed with the
sputum. But severe bleeding from the nose,
abundant haematemesis (vomiting of blood) or
haemoptysis (coughing up blood) is a very se-
rious problem which needs to be treated as an
emergency, second only to the establishment
of an adequate airway. We will not consider
here traumatic causes such as knife of gunshot
wounds or traffic accidents, which require a dif-
ferent approach, but restrict ourselves to ‘spon-
taneous’ bleeding. A patient may exsanguinate
effortlessly from bleeding oesophageal varices,
                                      The Basic ENT

a gastric ulcer or a pulmonary artery eroded by
carcinoma or tuberculosis.
         The first problem is to identify where the
bleeding is coming from.
      Pulmonary blood is usually easy to iden-
tify; bright red and foamy, invariably associated
with severe coughing episodes. This is usually
due to tuberculosis or a carcinoma which has
eroded a large artery, and there will be a history
of already diagnosed tuberculosis, or chronic
cough. In a bronchial carcinoma, the bleeding
may be the presenting symptom, but the patient
is generally older and has often smoked heavily
for many years.
      Bleeding from the digestive tract presents
as vomiting of (darker) fresh blood and ‘coffee
ground’ vomitus in varying quantities. Fresh
blood indicates that the bleeding comes from
the oesophagus, stomach or as far as the du-
      [In both haemoptysis and haematemesis,
some blood may pass via the nasopharynx
through the nose and be mistaken for epistax-

       Some basic studies are necessary to ob-
tain a fuller picture:

     A full blood count gives us an estimate of
how much blood may have been lost (as a rough
measure, every 500ml of blood lost reduces the
haemoglobin by 1mg, so a drop from 14 to 10
implies a loss of 1 1/2 to 2 litres). If there has
there been haemodilution the haemoglobin and
the haematocrit will be low, but it may take 12
to 24 hours after an acute bleed before this is
reflected in the peripheral blood. Beware of
the patient who has normal haematocrit and
normal haemoglobin after severe haemorrhage,
for his haemoglobin is likely to drop quickly
by dilution, even if there is no further haemor-
     It is important for us to know how long the
patient has been bleeding, especially in gastric
/ duodenal bleeds which tend to go unnoticed,
except for subtle clinical signs picked up only by
the most astute clinician. But any signs of im-
mature erythrocytes in the peripheral blood—
these take several days to appear—indicates
that the patient has probably been bleeding for
at least a week.
     Similarly, melaena, the tarry black stools
of partly digested blood usually take several
days to appear, and is likely to be present with
any important haemorrhage of the respiratory
                                     The Basic ENT

or digestive tracts.
     Chest auscultation will have been carried
out already, and there are usually sufficient
clinical signs to determine on which side of
the pathology lies, in case persistent bleeding
requires an emergency thoracotomy.
     Chest X-Rays are indispensable in se-
vere haemoptysis, for the affected pulmonary
segment may need to be resected. This is at
times the only possibility for saving the patient.
Perhaps in an advanced bronchial carcinoma
there is little gain, but tuberculosis is curable
with medication.
     In oesophageal varices there are usually
clinical signs of portal hypertension and liver
failure, perhaps with icteric sclerae and a his-
tory of hepatitis or alcoholism. Though the
varices are due to portal hypertension, the pres-
sure is rarely above 20mm hg and the bleed-
ing varices are easily occluded by the balloon
catheter of ..........
     But that is only a temporary measure, and
the varices will need to be ligated or the portal
hypertension reduced somehow by means of
shunt operations, (which often make the cer-
ebral symptoms of the failing liver worse). In
the absence of liver transplantation, it is a no-

win situation, but at least the patient does not
        Where available, flexible endoscopy
(bronchoscopy of gastroscopy) helps to identify
the bleeding site, but in a severe haemorrhage
there is too much blood to see anything, and we
still need to rely on clinical findings to delineate
the problem and initiate emergency measures
for saving the patients life.
The Basic ENT

     Bleeding from the nose is a common prob-
lem, and usually subsides spontaneously after
a few minutes, but occasionally it can represent
a serious medical emergency.
     The bleeding can originate anywhere in
the nose, more frequently on the nasal sep-
tum than the lateral wall. The vessels may be
either venous or arterial, and in young patients
the veins of Little’s area is usually involved.
Bleeding is almost invariably from a single ves-
sel, although trauma of repeated packing may
often give the impression of multiple bleeding
points. As a rule the bleeding is unilateral, and
consequently it is rarely necessary to pack both
sides of the nose, though since the blood in a
serious epistaxis often flows round the back
                                       The Basic ENT

of the septum via the nasopharynx and out
of the opposite nostril, a common mistake is
to think that both sides are bleeding. Simply
asking the patient which side started bleeding
first will determine where to look for a bleed-
ing vessel. Ignore the other side. The nose is
usually filled with clotted blood which should
be removed by aspiration, or asking the patient
to gently blow his nose to clear it. Then insert
a 5cm length of cotton wool, soaked in Xylo-
caine spray (10%) and a nasal vasoconstrictor
(neosynephrine, oxymetazoline, Adrenaline 1:
50,000 etc) into the nose. This is inserted as
far as possible into the nose (parallel with the
palate, not into the roof of the nose). After 5
minutes remove the cotton wool and carefully
examine the inside of the nose with a good head-
light or a head mirror reflecting a bright light. If
you can see the bleeding vessel it is an anterior
epistaxis and easily treated. If you cannot see
it is probably a posterior bleed and may cause
problems. The experience of the examiner is
of importance, but beyond a certain point, or
behind septal deviations, it is no longer possible
to directly see the bleeding point, and packing
is necessarily blind; depending more on luck
than skill. That is what makes the treatment

of posterior epistaxis uncertain.
    Different methods have been devised to
manage the bleeding.


     If the bleeding vessel can be seen (unless
actively bleeding it may be recognised as a small
red point lifted out of the mucosa, with often a
thin red ribbon leading to it) cauterise it with
silver nitrate or trichloracetic acid. If this is
not available, use electrocautery applied to the
vessel, taking care not to cauterise the nostrils
(the electrode must be covered with a length of
IV tubing leaving only the end exposed). Oth-
erwise a small pack of ribbon gauze is inserted
into the nose.

    Nasal packing is uncomfortable and the
nose must be well anaesthetised beforehand.
A length of ribbon gauze (a 1 inch roll of gauze
works well) is grasped 3 inches (+7 cm) from
the end with the bayonet forceps and inserted
along the floor of the nose (parallel with the
                                      The Basic ENT

palate and perpendicular with the face) as far
as possible — 4-5 inches (+10 cm). The gauze
is then grasped again 10 cm down and inserted
on top of the previous turn; gradually building
up the pack from the floor upwards until the
nose in filled with gauze. It is essential to build
up the pack in this way or it will loosen after
a short while. The most common mistake is
to pack into the roof of the nose which is very
painful and ineffectual except for bleeding from
the ethmoid vessels which is fairly unusual.
     Even a posterior bleed may often be ad-
equately controlled by a good pack. Beware
that if there has been some residual bleeding
into the pack, contraction of the clot after an
hour or so will force red serum out of the pack

and give the appearance of renewed bleeding.
Do not remove the pack unless there is frank
bleeding with clots. Always review the throat
after packing to see if there is no bleeding along
the posterior pharyngeal wall.
     Advise the patient that normal nasal se-
cretions will cause a bloodstained fluid to leak
from the nose until the pack is removed. Tell
him to keep his head above shoulder level for
the next few days and to avoid bending down,
or lifting heavy weights. Blowing the nose is
prohibited and he should keep his mouth open
when sneezing to avoid raising the intranasal
venous pressure.
     After 3 to 4 days the pack can be safely

    If a posterior epistaxis cannot be controlled
in this way, we may have to use a posterior
pack; an awkward and fairly ineffectual roll of
gauze which is pulled up through the mouth
into the nasopharynx. The technique of getting
the gauze into the nasopharynx is reminiscent
more of medieval torture chamber than of mod-
ern medicine, as most patients who have known
                                     The Basic ENT

this rare pleasure, will confirm. A canula is
passed through each nostril until they can be
grasped in the oropharynx with forceps and
brought out through the mouth. A gauze swab
is rolled up to a size of approximately 3x5 cm
and tied with silk sutures, leaving the ends
long. These ends are tied on to the canulas
which are then withdrawn through the nose.
The silk ties , one from each nostril, are pulled
tight to place the gauze in the nasopharynx
(often with the help of a finger in the throat),
and tied over small piece of gauze around the
     A simpler and more effective technique
is to use a Foley’s catheter of #14 or 16 and
pass it into the nose on the bleeding side until

the tip is seen below the soft palate. The bal-
loon is then inflated to 5 or 7 ml with air and
the catheter is drawn back until the balloon
is firmly wedged in the posterior choana on
the affected side. Maintaining tension on the
catheter, the anterior part of the nose is tightly
packed as described above around the catheter
and an umbilical clip or artery forceps is used
to fix the catheter on the nasal side while main-
taining slight tension. A piece of gauze should
be wedged between the clip and the nostrils to
prevent nasal skin necrosis. If the patient has
had no further bleeding for 24 hours, the bal-
loon can be deflated, but it is left in place for
several days and can be readily inflated again
if the bleeding recurs. After 5 days the vessel
is generally closed an the pack can be removed.
The patient is given antibiotics to cover infection
from the nasal flora and a tendency of the nasal
pack to produce sinusitis.

     A severe bleed can be temporarily stalled by
injecting 3 to 5 ml of Lignocaine with adrenaline
into the Pterygopalatine Fossa, via the greater
palatine canal. The latter is easily palpated
near the posterior edge of the hard palate on
                                     The Basic ENT

either side. Introducing a short needle into this
canal to a depth of 1 or 2 cm, the Lignocaine is
slowly injected into the fossa. This produces a
vasoconstriction of the internal maxillary artery
and its branches, and the bleeding stops. The
effect lasts up to 30 minutes, and gives us time
to explore the nose carefully and cauterise the
bleeding points or apply a good pack.

     Once in a while, usually in elderly patients
with hypertension, cardiovascular disease or on
anticoagulants, the bleeding is not controlled by
any of the above methods, and we have to resort
to more aggressive procedures. Ligation of the
Ethmoidal and Internal Maxillary arteries, or
the External Carotid artery.
     The internal maxillary artery is located
behind the posterior wall of the maxillary si-
nus and requires a microscope and specialised
instruments. Through an incision in the up-
per buccal sulcus, the periosteum is elevated
off the canine fossa as far as the Infraorbital
nerve, and the anterior wall of the maxillary
sinus is opened with a small gouge, to provide
a 1 square inch window into the maxillary si-
nus. The thin bone of the posterior wall is care-

fully fractured and removed, taking care not to
damage the vessels immediately behind. The
internal maxillary artery is identified, running
horizontally in the fat of the sphenopalatine
fossa, and clipped with neurosurgical clips. It
can be ligated but it is difficult to tighten the
knots in the confined space.
     The anterior and posterior Ethmoidal ar-
teries are approached along the medial wall
of the orbit via an incision in the eyebrow ex-
tended 2 cm along the edge of the nose. The
periostium along the orbit is elevated and the
medial orbital wall followed back until first the
anterior and a little further back the posterior
Ethmoidal arteries are encountered and ligated
or cauterised.
     If these techniques are inaccessible, go for
the external carotid.
     The external carotid artery is approached
via a neck incision anterior to the sterno-
mastoid muscle and slightly behind the large
jugular vein. Familiarity with neck anatomy
is required. Usually we encounter the com-
mon carotid first and follow it up to beyond
the bifurcation. This is always higher than
you expect (almost under the angle of the jaw).
Take time to identify at least two branches of
                                     The Basic ENT

the External Carotid before ligating it (this en-
sures that it is indeed the external carotid, as
the Internal Carotid has no branches in the
neck. Ligating the common or internal carotid
leads to hemiplegia in over 50% of the patients.
Once the arteries have been ligated, pack the
nose (there is sufficient collateral circulation
in the richly irrigated face to still allow some
bleeding). The incisions are closed in the usual
way. The anterior wall of the maxillary sinus
does not need to be reconstructed. I have not
known this method to fail, except in rare cases
where profuse bleeding from a gastric ulcer
or oesophageal varices produced such violent
vomiting that the blood running from the nose
and throat was mistaken for epistaxis.



      Foreign bodies in the external auditory
meatus (or outer ear canal) are common in
children who like to stick things they find into
any available orifice. They are often badly man-
aged, so that more damage is caused by the at-
tempted extraction than the foreign body would
ever have caused. While the object is in the
external canal there in no hurry in removing it!
It is not an emergency. At worst it can produce
an external otitis. So take your time, get any
necessary instruments and remove the object.
(For plant seeds I have heard it recommended
to wait for them to sprout and pull them out by
                                    The Basic ENT

the leaves, but that is perhaps too long)
     Forceps are not used for extracting objects
from the ear as it is too easy to push them fur-
ther down and damage the ear drum or middle
ear structures. First try using a small hook.
If an ear hook is not available make one from
a long hypodermic or Lumbar puncture needle
with the sharp point broken off, or a straight-
ened hairpin. About 2mm from the end it is
bent through 90º and you have an ear hook.
This is carefully advanced along the canal wall
past the foreign body, rotated to position the
hook behind the object (or in the eye of a bead
if possible), and carefully withdrawn. Take
care to rotate the hook towards the lumen of
the canal and not into the extremely sensitive
skin of the meatus. If there is not enough room
try syringing the ear. This usually dislodges a
foreign body even if it seems to block the canal
completely, as long as the stream is directed
towards the roof of the ear. The water should
be clean and warmed to body temperature (for
hot or cold water will make the patient dizzy
as we have seen in the vestibular tests for),
drawn up into a 20ml syringe with a large (14
or 16 gauge) endovenous canula attached and
injected into the external meatus. The stream

is directed obliquely upwards towards the roof
of the canal, not directly towards the drum
which can be damaged and perforated by a di-
rect stream. The water is allowed to run back
into a kidney dish which the patient or nurse
is holding under the ear. Repeated syringing
are usually necessary to remove large foreign
body or wax plug.


      A unilateral discharge from the nose of
a child is a foreign body unless proven oth-
      We will usually only have one chance to
remove a foreign body from a child, and unless
it is done carefully he will not allow anyone else
near him, so the removal has to be planned
      Clean the secretions from the nose and
spray a little 10% Xylocaine into the nose once
the foreign body has been located, to allow pain
free removal. Have the child (they are almost
always children), sit in its mother’s lap, with
one of her arms round his shoulders and arms,
and her other arm around his forehead, while
                                     The Basic ENT

his feet are firmly held between her knees.
This effectively immobilises the young patient
and prevents us from being kicked unexpect-
edly and painfully during the tricky moments
of the procedure. Pass a small probe, hook or
bent hairpin over the floor of the nose under the
foreign body. When the patient almost invari-
ably pulls his head back at this stage, the probe
levers the foreign body upwards and out of the
nostril. If we try to pass the probe above the
object, it will be levered deeper into the nose
or nasopharynx.
     A nasal foreign body as opposed to the au-
ral one, should be removed promptly, as it can
fall backwards during sleep and theoretically
be inhaled. However, I have not been able to
find any reports of pulmonary foreign bodies
which started out in the nose, so this is risk is
probably exaggerated, and we must allow some
credit to the larynx and pulmonary protection


     These are usually fish or chicken bones,
which tend to get stuck anywhere from the
tonsils to the Pyriform Fossa. The patient com-
plains of pain on swallowing vaguely localised
or lateralised which persists since the last meal
of fish or chicken.
     Use the laryngeal mirror and a good light
to carefully explore the whole of the visible area
down to the larynx.
     The fishbone often looks like a thin white
strand of saliva sticking out of the mucosa.
Once the foreign body has been located it can
usually be removed with local anaesthetic and
a little (patient) patient cooperation. Spray the
patients throat sparingly with Xylocaine 10%
and wait for 5 minutes. Then enlist the help
of the patient in holding his tongue (literally)
with a gauze. Insert the warmed mirror into
the throat as described earlier, and locate the
fishbone. Then use a Tilley’s forceps or small
McGill’s forceps to extract the bone. The only
trick is to get used to the inverted mirror image
which shows the instrument moving in the op-
posite direction to which we are moving it. Slide
the instrument over the base of the tongue helps
                                      The Basic ENT

to orient it in space, but it is useful to practice
once or twice with the mirror beforehand.
     If you are unable to remove it—sometimes
the patient does not cooperate— It is necessary
to use a short general anaesthetic. Only beware
that anaesthetists derive great pleasure in re-
moving the foreign body during the intubation
and triumphantly presenting it in the McGill’s
forceps, thereby effectively stealing the lime-


    Unless very small, these tend to cause stri-
dor and respiratory difficulty, and constitute
a real emergency. If a Heimlich manoeuvre
does not dislodge it, the patient needs to be
anaesthetised and the object is removed with
great care so that it is not pushed down into
the lungs. A direct laryngoscope and grasping
endoscopy forceps are best used for this. Chil-
dren under the age of one year are usually not
anaesthetised, and the laryngoscope is passed
directly to remove the object.


     These constitute a serious emergency and
should be removed as soon as possible, for
the object tends to move down the bronchial
tree (with preference for the right side which is
straighter) until it obstructs completely, leading
to rapid atelectasis and a whole series of pulmo-
nary problems. The patient initially has violent
coughing fit but then becomes asymptomatic
until infection sets in behind the obstruction.
     A flexible bronchoscope may help in the
diagnosis, but for larger objects it is better
to use a rigid bronchoscope for removal. For
round and slippery objects, a urological basket
catheter can be tried.


     These are usually fish or animal bone or
meat, but almost any object known to man
(within certain structural limits) has been re-
moved at one time or another. The patient has
a clear story and has usually tried eating bread
or banana etc. to try to dislodge the foreign
body. Though usually with the foreign body
                                     The Basic ENT

suspended, the oesophagus becomes paralysed
and the patient is not able to swallow, this is
not always the case. Often the piece of bone
has moved down and left a small laceration in
the oesophagus which is painful during swal-
lowing for some days. When there is doubt and
the patient is swallowing, have him come back
after 2 to 3 days when any scratch or ulcer will
have healed. Should discomfort persists he will
need an endoscopy. Obviously a radio opaque
bone will show up on X-ray and there may be
some air trapped in the oesophagus above a
non opaque object which may show up on the
lateral neck or chest x-ray.
    Rigid oesophagoscopy is a dangerous pro-
cedure and should only be carried out under
expert supervision, for a perforated oesophagus
leads swiftly to mediastinitis and may prove
fatal. It is however the quickest and least trau-
matic way of removing a large foreign body.


     Pain in the ear must be carefully explored,
as the possible aetiology is very varied. Is it as-
sociated with hearing loss? or dizziness? then
the cause is likely to be in the ear. If the ear
seems normal, examine the surrounding struc-
tures. Tonsillitis frequently refers pain to the
ear, while pathology of the temporomandibular
joint and dental pathology is often experienced
as pain deep in the ear. Examine the ear from
pinna to drum by direct examination, and via
the various functional tests mentioned above,
for labyrinth symptoms. The pain can be either
direct or referred, but the innervation of the ear
is extensive and unusual, so that a number of
nerves must be taken into account:
     Trigeminal (V—the main nerve to the
external canal), Facial (VII—strictly a mo-
                                     The Basic ENT

tor nerve, but often containing a tiny sensi-
tive branch hitchhiking from the tympanic
plexus), Glossopharyngeal (IX—via a branch
called Jacobson’s nerve supplies the middle
ear and tympanic plexus), Vagus (X—sends a
small branch called Arnold’s Nerve to the pos-
terior part of the external canal, which causes
coughing when the ear is scratched or cleaned),
Accessory (XI—supplies most of the fibres for
Arnold’s nerve), C2&3 (Greater Auricular and
Lesser Occipital nerves—main innervation to
the pinna)
     Referred pain must explore all possibilities
along these lines; looking for pathology from the
base of skull to the neck and vertebral column,
and as far foreword as the maxillary sinuses
and nose. Referred pain may originate from
pathology anywhere along any of the nerves
which supply the ear, just as hitting the elbow
causes tingling in the little finger and hand.

       Infections and inflammations of the ear
are conveniently subdivided for the sake of clar-
ity into otitis externa, myringitis, otitis media,
mastoiditis and labyrinthitis.

     Otitis externa may involve any part of the
outer ear up to the ear drum. Since this is an
extension of the skin, it is essentially a dermato-
logical problem; a dermatitis, involving bacteria
from the skin flora, as opposed to the middle
ear and mastoid which are extensions of the up-
per respiratory tract and become infected with
bacteria from the airways. While the eardrum
is intact at least, the two are entirely separate.
But a perforation of the drum quickly spreads
resistant skin flora into the middle ear.
     Since the external meatus is largely con-
tained in a bony or cartilagineous canal, any
                                    The Basic ENT

inflammation has little room for expansion and
the canal tends to swell inwards, gradually clos-
ing itself up.
     The restricted expansion often produces
severe pain, especially when the canal becomes
completely closed off, and a blocked sensation
in the ear.
     There is pain on moving the Pinna and while
chewing, and a slight, watery discharge mixed
with squamous debris. In otitis media there
may also be severe pain, but it is not affected
by movements of the pinna or mastication. An
abundant mucoid discharge can only come from
the mucous glands of the middle ear and always
indicates a perforation of the ear drum and in-
volvement of the middle ear.
     External otitis is often caused by swimming
when water remains in contact with the meatal
skin for prolonged periods of time. The skin
gradually becomes excoriated, and the normal
skin flora is able to penetrate the defences and
produce an infection. Although the pain is of-
ten severe, the infection is not dangerous as it
is effectively isolated from the middle and inner
ear structures by the ear drum. The ear needs
to be cleaned out with a Jobson probe or orange
stick wound with a small wisp of cotton wool.

This has to be done gently as the swollen tis-
sues are very tender. The ear is then filled up
with antibiotic ear drops or dusted with antibi-
otic powder. However, one of the most effective
forms of treatment is to fill a 3 ml syringe with
a broad spectrum antibiotic eye ointment or
dermatological cream, which is then carefully
injected into the ear canal, taking care not to
scratch the canal with the needle; or better still,
using the plastic intravenous canula already
mentioned for syringing foreign bodies. Usu-
ally a single application lasts 3-4 days and is
sufficient to cure the infection. Acid ear drops
(50% vinegar and 50% boiled water are also
very effective
     Once the swelling of the external meatus
goes down the canal and eardrum are carefully
inspected for signs of other pathology.

    Necrotizing otitis externa

     This deserves a separate mention. In the
immunocompromised, diabetic or elderly pa-
tient, a Pseudomonas related infection of the
external ear may spread very quickly, in a mat-
ter of days, to the base of skull. There is severe
                                     The Basic ENT

pain and slight ear discharge. The infection
often causes a facial palsy initially and grad-
ually takes off other cranial nerves as the base
of skull is reached. Treatment is a combination
of careful control of the diabetes (if the patient
has diabetes), antibiotics to which the Pseu-
domonas is sensitive, and often surgical debri-
dement. Prognosis is poor once the skull base
has been reached, so it is important to think
of this pathology when encountering an exter-
nal otitis in a diabetic or immunocompromised
patient, and treat aggressively with broad spec-
trum antibiotics. The problem is analogous to
foot infections in diabetics.


     On the border between external otitis and
otitis media, is the inflammation of the ear drum
itself. Though frequently involved to some de-
gree in both otitis media and otitis externa,
there is a specific condition which affects prin-
cipally the ear drum. This is known as bullous
myringitis, and the drum is covered with one or
more haemorrhagic bullae, at times extending
onto the external canal wall which is otherwise

normal. The condition is of viral origin, usually
associated with a cold or flue, and is excruci-
atingly painful. If a bullae bursts there may
be a little bloodstained discharge from the ear.
The condition is self limiting and requires only
symptomatic analgesic. Occasionally the whole
thickness of the drum may be involved, leaving
a large perforation which does not tend to heal
spontaneously. Normally, the bullae gradually
heal and dry up.

    Otitis Media

     There are three basic types: Acute otitis
media, secretory otitis media and chronic sup-
purative otitis media.
     The pathophysiology is similar to sinus
disease. Generally there is an initial viral up-
per respiratory tract infection which produces
swelling of the Eustachian tube, so that air does
not reach the middle ear as it normally does
to maintain equal pressures on either side of
the ear drum. The middle ear cavity is closed
off and the oxygen within it is absorbed by the
cells. As the partial pressure of the gas drops,
the drum is drawn inwards, with an intermit-
                                    The Basic ENT

tent blocked sensation and often pain. The
middle ear then fills up with fluid, increasing
the blocked sensation. This fluid produces the
secretory otitis media, and may take several
weeks to reabsorb. In children under the age
of eight, due to the anatomical condition of the
eustachian tube, coupled with an immature
immune system and often the use of systemic
decongestants with pseudoephirine, the fluid
gradually thickens and may remain in the ear
for months at a time, or even longer if a subse-
quent viral infection supervenes. This is what
is known as chronic secretory otitis media
or “glue ear” for its resemblance to the sticky
transparent paper glue often used in schools.
     If the secretions become infected (which is
not difficult, as it is an ideal culture medium
for human pathogens), it leads to empyema for-
mation within the middle ear cavity, or acute
suppurative otitis media. The empyema
causes gradual bulging of the ear drum, with
rapidly progressive pain. The bulging of the
drum interferes with its delicate blood supply
and leads to a central necrosis which eventu-
ally perforates, allowing the pus to discharge
to the outer the canal, with immediate pain
relief. Sticky mucoid pus, slightly bloodstained

initially, begins to drain from the ear, but the
child who minutes before had been scream-
ing with pain becomes quiet and quickly falls
asleep. Once the pus has been discharged, the
middle ear mucosa is often able to control the
infection and the secretions dry up. The drum
will usually heal spontaneously in the course
of a week or two.
     Acute otitis media ideally should be treat-
ed with decongestant nose drops and antibiotics
before the drum perforates. The nose drops
decongest the nose and the Eustachian tube
and thus hopefully reverse the condition which
led to the otitis in the first place. This nasal
decongesting is one of the most important com-
ponents of the treatment of acute and secretory
otitis media, but is often overlooked. Even the
patient often finds it slightly ridiculous to be
putting drops in his nose when it is obviously
his ear which is giving him all the problems
and the pain. Unless this is carefully explained
he may even put the nose drops in his ear.
The antibiotic requires 12 to 24 hours to start
having effect, so for severe pain and a bulging
hyperaemic drum it is sometimes convenient to
make a small controlled incision (in the antero-
inferior quadrant of the drum) and let the pus
                                     The Basic ENT

escape, rather than risk a large and possibly
non-healing perforation. The myringotomy as
this is called should be restricted to the anterior
inferior quadrant to avoid damage to the ossi-
cles or round and oval windows. It consists in
a small stab incision made with a myringotome
of a large hypodermic needle. The drum may
be anaesthetised beforehand with a 10% xylo-
caine spray which is surprisingly effective on an
inflamed drum. Under normal circumstances,
a myringotomy will heal in 3 to 4 days without
leaving a scar.
     Once a drum has perforated spontaneously,
there exist two possibilities. It will heal within
a week or two, or a perforation will remain. If
the middle ear mucosa meets the outer ear skin
before the perforation has been bridged, there
is no further tendency towards healing. This
often occurs if the middle ear abscess becomes
contaminated with skin flora, and the infection
is maintained for some time. The prolonged
discharge prevents the perforation from being
adequately bridged. It is important therefore
to provide adequate antibiotic coverage and ear
cleaning after a spontaneous perforation.
     If after being perforated the ear remains dry,
or uninfected, there is only a mild to moderate

hearing loss (maximal 40-50%). But, as so
often happens especially in circumstances of
poor hygiene, the middle ear becomes infected
through the perforation, it becomes a chronic
problem, or chronic suppurative otitis media.
This is really a series of recurrent infections of
the middle ear mucosa via a perforated drum;
a small amount of contaminated water reach-
ing the middle ear via the perforation, will
start the process up again, gradually leading
to hypertrophic changes of the exposed middle
ear mucosa and chronic discharge.
     The ear needs to be carefully mopped, as
in external otitis or gently syringed with saline
solution (at body temperature) to remove as
much secretion as possible, after which anti-
biotic drops are instilled twice a day, filling up
the ear canal completely. Use the drops lib-
erally (10-15 drops), for 2-3 drops three times
per day as is usually indicated barely moistens
the external meatus, and does not reach the
middle ear mucosa. Though many of the ear
drops contain ototoxic antibiotics they may be
safely used in the middle ear while the mucosa
is swollen, but should be stopped within 2 days
of the ear becoming dry. An ophthalmological
antibiotic ointment is also very effective, and is
                                     The Basic ENT

used to fill up the ear completely (after cleaning)
and left for some days. Once the infection dries
up usually after 5 or 6 days, the trick is to keep
the ear dry. The patient should use a plug of
cotton wool covered in vaseline for bathing, and
avoid blowing his nose. This is another point
which is often overlooked, for blowing the nose
with a perforated eardrum produces sufficient
pressure to push the infected nasal mucus and
bacteria into the middle ear (an intact eardrum
normally provides sufficient counterpressure
to prevent this). That is also the mechanism of
spread for the occasional tuberculous otitis me-
dia which is in my experience always secondary
to pulmonary tuberculosis.

    Cholesteatoma is an epithelial retraction
cyst invading the middle ear. Though essentially
a benign condition, within the bony confines of
the middle ear it behaves destructively, often
damaging the ossicular chain and extending into
the mastoid region. The bone of the inner ear
and labyrinth may be eroded, producing peril-
ymph fistulas and episodes of vertigo. There is
progressive deafness, conductive initially as the
ossicular chain is destroyed, and then sensory-
neural with the exposure of the inner ear. The

facial nerve may also be exposed, but there
is rarely facial paralysis. Sooner or later the
squamous debris trapped within the cyst be-
comes infected, producing a scanty foul smell-
ing discharge. The diagnosis may be made on
the basis of the typical smell, likened to that of
a nest of field mice or the feet of athletes. The
infection further damages the inner ear func-
tion and may lead to meningitis. The treatment
is surgical and consist in complete removal of
the cyst.

     Mastoiditis is the most serious ear con-
dition of those mentioned so far, and consists
of extension of the middle ear infection into
the mastoid aircell system. The narrow canals
of the system quickly become blocked with the
mucosal swelling, and abscesses form within
the cells, leading to pain behind the ear and
fever. There is always concomitant otitis media
with a hyperaemic drum and typically a small
perforation with a little purulent secretion. The
danger of mastoiditis is that the abscess forms
deep within the mastoid bone, and is under
pressure to find a way out. This may be via the
middle ear and drum, but it may also present
as a painful swelling behind the ear under the
                                     The Basic ENT

periostium of the mastoid bone. Both of these
may drain spontaneously to the outside, but in
an unlucky patient the abscess finds its way
inwards, producing meningitis or a brain ab-
scess. Conversely, any patient presenting with
meningitis or cerebral abscess must have his
ears carefully inspected, for an otic meningitis
or cerebral abscess may not be curable without
clearing the infection from the mastoid. This is
done via a mastoidectomy, in which the mastoid
bone is drilled open and cleared of infection.
This is a specialised procedure, with risk to the
inner ear and facial nerve, and should not be
attempted by the novice. The only emergency
procedure which is occasionally successful is to
‘uncap’ the mastoid by removing with a gauge
or bone forceps, only the cortical bone so that
the abscess may drain outwards.
    There is now such a wide selection of good
broad spectrum antibiotics available that an
early “uncomplicated” mastoiditis may be safely
and successfully treated without surgery. The
middle ear secretions are drained through a
wide myringotomy (take a culture of the secre-
tions before starting antibiotics) and the patient
started on broad spectrum antibiotics. Quinolo-
nes are a good choice, but chloramphenicol also

works well if cost is an issue, for the treatment
must be continued until there is no more se-
cretion from the middle ear, and the ear drum
looks clinically normal. Where available, CT
scans are the best way of assessing whether
the infection has completely cleared up, but
the patient is kept under periodic observation
for several months.
     If the infection finds its way into the inner
ear, it is known as labyrinthitis. Initially only
the bacterial toxins of the surrounding infection
penetrate to the labyrinth, inducing an inflam-
matory reaction (serous labyrinthitis) with ver-
tigo and an irritative nystagmus towards the
affected ear, with variable hearing loss. This
condition is still largely reversible, but should
the infection progress to pus formation in the
labyrinth (suppurative labyrinthitis) there
will be irreversible destruction of the inner ear
neuroepithelium. The patient has very violent
vertigo, nausea and vomiting, with nystagmus
towards the opposite ear, severe to total senso-
ry-neural deafness, and often intractable tinni-
tus. Though the vertigo gradually compensates
within a few weeks to months, the hearing never
recovers. There is a high risk of meningitis and
cerebral abscess formation. Both serous and
                                    The Basic ENT

suppurative labyrinthitis should be treated like
     All patients with suppurative otitis media
should be kept under careful observation, for
the complications include: mastoiditis, labyrin-
thitis, extradural abscess, subdural abscess,
meningitis, venous sinus thrombosis of the
sigmoid sinus, and brain abscess, facial nerve

     Vertigo and dizziness are often indistinctly
used, but vertigo is a sensation of rotation or
movement (either the patient feels he is whirling
round, or that the room spins around him) while
dizziness is a general feeling of unsteadiness
without a sensation of movement. Dizziness is a
vague symptom occurring with many illnesses,
but true vertigo is generally caused by a lesion
in the vestibular pathways or brain stem.

    Vertigo may be of central origin (brainstem,
cerebellum) or peripheral (inner ear and ves-
tibular nerve connections)

       The brainstem integrates information not
only from the inner ear labyrinths on either
side, but also from the eyes and from the prop-
                                     The Basic ENT

rioceptive receptors in the joints and muscles of
the body, and especially those of the neck. This
allows us to determine our position in space and
accurately balance posture and movements.
     Peripheral vertigo must be distinguished
from central causes, which on the whole have
a more serious prognosis.
     The history and examination usually enable
us to locate the site of the problem.
     Peripheral vertigo is typically of sudden
onset, short duration, or variable, associated
with deafness, tinnitus or ear discharge. There
is often nausea and vomiting and a marked
nystagmus. There should be no associated
Central Nervous System symptoms and cra-
nial palsies, but the caloric test is diminished
on the affected side.
     Central vertigo is often of gradual onset,
continuous and progressive, with associated
C.N.S. symptoms as headache, papilloedema,
ataxia or cranial nerve palsies. Otological signs
are infrequent and the caloric response is usu-
ally symmetrical.
     Central causes belong to in the area of
neurology and neurosurgery and will not be
discussed here.
     Peripheral vertigo is seen in labyrinthitis,

discussed above, in vestibular neuritis or neu-
ronitis, in labyrinthine concussion after trauma,
with ototoxic medication such as Streptomycin
and Gentamicin, Meniere’s disease and a neu-
roma of the acoustic nerve.

     There is also a condition known as Benign
(paroxysmal) positional vertigo or BPPV. This
is probably the most common of the vertigo's and
causes intermittent vertigo associated with head
position. The vertigo is self-limiting and lasts
up to several minutes gradually diminishing.
Changing the head position may produce an-
other episode of short duration. This problem
has been attributed to some of the microscopic
calcium crystals (otoliths) from the inner ear,
becoming detached and floating through the
endolymph onto the delicate neuroepithelium
of the semicircular canals, producing a stimu-
lus of movement. The model goes a long way
to explaining the problem, and various simple
manoeuvres have been designed to rotate the
patient in such a way as to float the crystal into
another part of the labyrinth where it will cause
no problems.
     Meniere’s disease, is a rare disease which
is commonly diagnosed, is the otological equiv-
                                     The Basic ENT

alent of glaucoma; an intermittent increase of
pressure in the inner ear which causes damage
to the delicate structures. There is fluctuating
hearing loss (worse initially then gradually im-
proving), tinnitus and severe vertigo with nys-
tagmus. Episodes occur at intervals of weeks
to years and there is spontaneous recovery in
the course of several weeks. Repeated episodes
usually leave some residual damage to the hear-
ing and vestibular apparatus.
       Many drugs can cause damage to the
inner ear (ototoxic drugs), but the most
notorious are the aminoglycoside antibiotics
(Streptomycin, Gentamicin, Kanamycin) which
are selectively absorbed by the inner ear and
attain high concentrations. The damage is
furthermore permanent and irreversible, so
that once the patient complains of symptoms;
vertigo, deafness and tinnitus, it is already too
late. These antibiotics are best avoided as far
as possible, for even careful dosage is not suf-
ficient to ensure safety, and they should really
only be used in life threatening illness (such as
meningitis) and if possible with control of serum
levels especially if there is poor renal function.
The vertigo is severe and long lasting, with often
incomplete compensation. The only treatment

is to suspend the medication immediately and
give corticosteroid therapy (1 mg/kg/day) for 10
days. Take great care with tuberculosis patients
who are often given an adult dose of Streptomy-
cin calculated for a 70Kg adult, while they often
weigh only half that, thus ensuring overdose.
Ototoxic deafness and vertigo is particularly
common there.
     Vestibular neuronitis is an inflammation
of the vestibular labyrinth or nerve, frequently
associated with a viral upper respiratory tract
infection. There is a severe incapacitating ro-
tational vertigo which gradually improves over
a few week as the complex brainstem compen-
satory mechanisms take effect. There may be
lasting damage to the labyrinth (diminished ca-
loric response) but compensation is generally

       Any damage to the inner ear affects the
balanced impulses reaching the brainstem, and
produces a hallucination of movement already
mentioned which can be severe enough to ac-
tivate vagal reflexes of nausea and vomiting.
     There are complex mechanisms to recover
the balance, as the brainstem desperately
tries to recalibrate and compensate for the
                                     The Basic ENT

asymmetrical or deficient information. In the
initial acute phase we may use labyrinthine
suppressers such as Dramamine or Vontrol.
These are tailed off after a week, and the pa-
tient is started on neck exercises, so that the
brainstem receives all the necessary informa-
tion for compensating the deficient vestibular
information; to be able to reset the bodies equi-
librium. A frequent cause of vertigo persisting
long after a peripheral episode, is that the pa-
tient avoids certain movements which produce
his vertigo, so that these movements are never
adequately compensated in the brainstem, and
unsteadiness in those positions may persist for
years. The exercises are therefore essential, ir-
respective of the origin of the peripheral vertigo
as soon as the acute episode has passed (one or
two weeks). They consist in having the patient
(sitting down, to avoid falling), moving his head
through the different positions—nodding ‘yes’,
shaking ‘no’ and rotation in both directions—
for about 10 to 15 minutes every evening. If
he discovers any position or movement which
produces vertigo this rather than being avoided,
should be exercised more, to allow the brain-
stem to compensate. Normally within 2 weeks
there is a dramatic improvement, though the

patient must be warned of occasional relapses,
especially related to stress and fatigue. After
several months, depending partly on the age
of the patient (less in children, more in the
elderly) there should be a complete compen-
sation. The brainstem is able to compensate for
the complete loss of one labyrinth. If there is
inadequate compensation, other causes should
be explored, and central vertigo must always
be kept in mind. In Meniere’s syndrome it is
sometimes difficult to achieve compensation,
due to its fluctuating nature.
The Basic ENT

     Deafness is often thought of as an all or
none phenomena, whereas in fact complete
deafness is rare, so it is better to talk of hear-
ing loss, which is measured in decibels; from a
normal hearing of zero to twenty, to ‘complete
deafness’ at around 120 dB.

     We consider the first 20 or 30 dB to be
within normal limits, and the patient normally
does not complain. From 30 to 60 dB is a mod-
erate hearing loss which is more of a problem
for family and friends, who have to raise their
voice to be understood by the patient. Above 60
dB the patient begins to suffer communication
problems, until above 90 or 100 dB he is for all
practical purposes unable to hear anything.
                                     The Basic ENT

    If severe deafness occurs before language
development, as in childhood meningitis or con-
genital deafness, during the first years of life,
the child is unable to develop normal spoken
language except through very rigorous train-
ing, and even then will develop it imperfectly.
Post-linguistic deafness also leads to a dete-
rioration of the speech though lack of auditory
    Hearing loss can be due to conductive or
sensory-neural causes.

     Conductive hearing loss is due to any
problem in the outer or middle ear, which pre-
vents the sound waves from reaching the inner
ear; wax in the external canal, fluid in the mid-
dle ear, a perforated drum, otosclerosis. The
maximum loss of hearing in a purely conductive
deafness is about 50% or 50dB (on a logarithmic
scale from 0 to 120 dB which are the limits of
intensity we can comfortably hear), above which
sound reaches the inner ear directly via bone
conduction through the bones of the skull. The
sound is generally perceived as normal in qual-
ity but diminished in intensity.

    Sensory neural hearing loss is the result

of a defect or damage in the inner ear or au-
ditory pathways (from cochlea to cortex) It fre-
quently associated with tinnitus, and there may
be distortion of the sound quality. The degree
of loss may be partial to complete.
     Partial loss is common with old age (pres-
bycusis is the auditory equivalent of presbyopia
of the eyes) and due to exposure to loud noises
or rock music

      Tinnitus Is a hallucination of sound which
is usually, but not invariably associated with
a sensory neural hearing loss. The inner ear
generates impulses (independent of incoming
sound waves) which the cortex interprets as
sound. Through psychological feedback it can
attain unbearable proportions at times, but if
the patient can be persuaded to take his mind
off it he will gradually become accustomed to it.
This is not as simple as it sounds, for it is like
asking the patient not to think of for instance
pink elephants; he will literally not be able to
keep his mind off them. But distraction tech-
niques are used to make the patient think of
other things or listen to music which tends to
mask the tinnitus.
                                    The Basic ENT

       Tuning fork tests, history and exami-
nation of the ear, allow us to distinguish be-
tween conductive and sensorial hearing loss
(the former usually reversible, while the latter
is always more serious and more intractable to
treatment). Furthermore, the conductive hear-
ing loss can never exceed 50 dB (+50% loss)
while a sensorial damage may mean complete
deafness, and is often irreversible, for we have
no way of repairing damaged hair cells in the
organ of Corti, or a spiral ganglion neurones.
A severely deaf patient cannot hear the tuning
forks, but by positioning ourselves behind the
patient and clapping or shouting loudly, we can
judge his reactions (or lack of them). Make
sure he cannot see you, for the innate human
language drive is so strong that most severely
deaf patients learn to lip-read. Young patients
often become so competent at this that they
miss very little of a normal conversation as long
as they are facing the speaker.
       Severe hearing loss or total deafness is
a rare but serious complication of meningitis,
mumps or measles virus, usually in child-
hood, the patient gradually loses any speech
he may have had, for auditory feedback is es-
sential for normal communication and speech

development. There are rare cases of congenital
deafness either from birth or progressive during
the early years of life, but it may also be caused
by a severe meningitis or to an intoxication with
aminoglycoside antibiotics (Streptomycin, Gen-
tamicin, Kanamycin) or occasionally quinine
compounds as mentioned in the chapter on
vertigo. Often associated with tinnitus and oc-
casionally with vertigo due to affectation of the
posterior labyrinth.
     Conductive hearing loss is usually amenable
to treatment: wax is syringed from the ear, otitis
media treated and the perforated drum grafted.
Even damaged or fixed middle ear bones may
be replaced or corrected with considerable suc-
     Sensory-neural hearing loss however is usu-
ally not treatable, with the exception of a sudden
onset hearing loss in its early stages (first few
weeks), when a short course of corticosteroids
often helps to reverse the hearing loss. Starting
with 1 mg/Kg/day tailed off in 5mg intervals in
the course of 2 weeks.
     For partial deafness a hearing aid helps to
amplify the incoming sound sufficiently for the
patient to hear.
     A severe sensory-neural deafness requires
                                   The Basic ENT

specialised treatment especially in children if
they are not to lose their language and com-
munication abilities, and these children should
be referred early on to a school or centre for
the deaf.

       Facial expression is such an important
part of nonverbal human communication, that
any paralysis or even deficiency of facial move-
ments tends to not only be immediately no-
ticeable, but provide a serious social stigma for
the patient. Paralysis is due to the interruption
of the facial nerve along its long course through
the temporal bone or in the face. The most
common ‘cause’ is idiopathic Bell’s Palsy for
which no clear cause has been shown, although
there is a frequent association with viral upper
respiratory tract infection. Another important
cause of facial paralysis is ear surgery—iatro-
genic damage to the nerve during mastoid or
middle ear surgery. Severe head trauma may
result in fractures of the temporal bone which
                                     The Basic ENT

can involve the nerve. Inflammatory processes
in the middle ear and mastoid may affect the
facial nerve, or more commonly, a viral proc-
ess causes inflammation of the nerve so that
it squeezes closed its own blood supply by
expanding within the restricted bony canal,
leading to variable degrees of neural damage.
Herpetic lesions in the outer ear or in the throat
should lead us to suspect a Herpes Zoster in-
fection which has a far worse prognosis (more
than 50% are permanent) than the Bell’s palsy
which is often associated with an over 95% re-
covery. Surgical decompression of the nerve is
often recommended, but it is a difficult surgery
even in expert hands, and has not been able
to show better results than conservative treat-
ment except in traumatic or iatrogenic damage
to the nerve. Of the many possible treatments
which have been recommended at one time or
another, the only one which has stood the test
of time is a short course of cortisone. Bear in
mind that it is always difficult to assess clini-
cal results in a pathological process of which
we do not understand the aetiology and whose
outcome is so unpredictable (there is frequently
a spontaneous recovery). All we can say is that
it is an empirical therapy which seems to work

in a good number of cases and has few undesir-
able side effects or complications. 1 mg / Kg /
Day in a single morning dose, tailed off by 5mg
daily to zero in 2 weeks is the scheme I usu-
ally use. Facial paralysis is an unsatisfactory
pathology to treat, and the results of neural
reconstruction are unsatisfactory. Fortunately
spontaneous recovery is common.
The Basic ENT

        Nasal obstruction is probably one of the
most common symptoms in medicine. Espe-
cially if we consider that under normal circum-
stances one side of the nose is partially blocked
by swelling of the inferior turbinate while we
breathe principally through the other side (this
is reversed every 4-5 hours. This is known as
the nasal cycle.
     Therefore a patient who complains of alter-
nating obstruction usually has some problem
which produces increased swelling of the nasal
mucosa, such as an allergic, vasomotor or viral
rhinitis or a sinusitis (in children , enlarged
adenoids are often blamed, but they suffer
more often from an allergic rhinitis). A persist-
ent unilateral obstruction may be caused by a
deviation of the nasal septum, a foreign body in
the nose or a nasal polyp or tumour and very
                                     The Basic ENT

occasionally a choanal atresia.
     Watery rhinorrhoea and sneezing are typi-
cally symptoms of the allergic vasomotor or viral
rhinitis, while purulent rhinorrhoea, postnasal
secretion and intermittent facial pain indicate
a bacterial rhinitis or sinusitis.

      This is an inflammatory process in the
paranasal sinuses (maxillary—in the cheeks,
ethmoid—between the eye and the nose, fron-
tal—under the forehead, sphenoid—below the
hypophysis) Any of these air filled cavities may
become involved. The usual sequence of events
starts with a viral URT infection; a cold or a
flue. Inflammation of the nasal mucosa not
only causes nasal obstruction, but also blocks
the small ducts or ostia, leading to the sinuses.
The result is an air filled cavity closed off from
the outside. Within this cavity, the oxygen is
absorbed by the tissues and cells lining the
sinus, leading to a rapid drop in the partial
pressure of the air in the sinus. This partial
vacuum is painful and gives the uncomfortable
ache in the face and head often associated with
a cold. If this low pressure persists for any
                                     The Basic ENT

length of time, the sinus fills up with a mixture
of transudate induced by the low pressure, and
excessive secretion induced by the virus. There
is a temporary improvement in the symptoms.
But the fluid in the sinus is an ideal culture
medium, and rapidly becomes infected by the
nasal flora, so that it is converted into an ab-
scess. The facial pains return, especially on
bending down, and there is pain in the upper
molars, whose roots run close to the maxillary
sinus floor. An X-ray at this stage shows the
typical fluid level in the maxillary sinuses.
     The nasal secretions then turn yellowish/
     Since the infection causes more inflam-
mation, and the inflammation does not permit
the sinus to drain properly, a vicious circle is
established which maintains the chronic proc-
ess active. Complications which can include
orbital or cerebral abscess, are fortunately very
     [The most useful x-ray is the simple ‘Wa-
ters’ view—chin against the plate—, the full si-
nus series is usually an unnecessary expense
for establishing a diagnosis, unless there are
     Treatment is directed at clearing the infec-

tion with antibiotics and decongesting the nasal
mucosa to allow healing prevent relapse. Ampi-
cillins or Co-Trimoxazol are useful antibiotics,
but they must be combined with decongestant
drops and continued during several weeks, or
the sinus ducts do not open and the process
simply relapses with other bacteria resistant
to the antibiotic.
     A sinusitis associated with foul smelling
pus and secretions is almost invariably due to a
dental abscess of the upper molars, which has
perforated into the maxillary sinus. Typically
the process is unilateral. Once the dental prob-
lem has been treated the sinusitis clears up.
     Occasionally several courses of antibiot-
ics are needed to improve the sinusitis and
the decongestant drops (adrenaline 1:50,000,
oxymetazoline, neosynaphrine), which after a
week are changed to simple drops of distilled or
plain boiled water, should be used three times
per day for a month.
     The majority of sinus problems do not re-
quire surgery. But occasionally, a long-stand-
ing problem has resulted in the sinus filling up
with polyps, cysts and inflamed mucosa which
no longer responds to medical treatment. The
sinus (Maxillary usually) then needs to be
                                     The Basic ENT

cleared out by surgery. The other indication
for surgical drainage is intra-orbital extension,
which is more common in children or intrac-
ranial complications—fortunately very rare.
     A final important point, sinusitis does not
cause swelling of the face (except in orbital
complications). Sinus symptoms with facial
swelling therefore, indicates a dental abscess
or a tumour.

       Headache is usually discussed under
neurology, but the causes are more frequently
otolaryngological than strictly neurological, so
we will give a short breakdown of the different
types of headache encountered from time to
time. Contrary to popular concept, a head-
ache, even a severe one does not imply a ‘brain
tumour’; in fact the majority of brain tumours
do not present with headaches, so that papil-
oedema on fundoscopy is a more specific find-
ing. Similarly, the clinical history is far more
important in diagnosing a headache than any
studies, including CT and MRI scans which
even where they are freely available more of-
ten than not come back ‘negative’ (the so called
scan negative headache)
     The great majority of headaches are ‘idio-
pathic’ —we never find out a clear cause—self
                                     The Basic ENT

limiting, and of short duration, so that initial
treatment should always be symptomatic.
     A true migrainous headache is not com-
mon, and is usually characterised by typical
aura or by visual scotoma and marked photo-
     Cluster headaches, similar to migraine
but without the aura or scotoma are more
common, and tend to occur in batches after
which they may disappear for months or even
longer. Their cause is often unclear, but reac-
tion to foods such as chocolate , coffee or strong
cheese should be explored as allergic causes.
An association with the menstrual cycle places
it among the hormonal causes.
     Sinusitis, as we have already seen causes
headache especially in its initial phase and
during acute infection, but may cause only
occasional pain in the chronic phase. Chil-
dren especially, tend to complain little about
     Sluder headache is triggered by the nasal
turbinates pressing against a deviated nasal
septum or septal spur and is cured by cor-
recting the deformity. It may be tested by ap-
plying anaesthetic and vasoconstrictor to the
nose during the initial stages of the headache,

and confirmed by making it disappear (though a
recent study has shown that spraying the nose
with xylocaine is helpful in migrainous head-
aches also as long as it is done early enough).
     Neck problems may cause a cervical head-
ache, typically in the occipital part and top of
the head, which is also the common site of ten-
sion headache due to the tense cervical muscles
pulling on their cranial insertions, or trapping
the occipital nerves as they pierce the muscles.
This produces very localised tenderness and is
cured rapidly by local heat or a small injection
of Lignocaine.
     High blood pressure rarely causes symp-
toms, but should be excluded.
     True neurological causes include men-
ingitis, (bacterial or viral) with signs of neck
stiffness which though subtle initially, must be
identified in the early stages.
     Parasitic infections such as Malaria and
Amoebiasis are often associated with head-
     Rarer causes may be reviewed in the rel-
evant neurological texts, if initial symptomatic
treatment and a little ‘Tincture of time’ have not
yield results.
     Obviously the psychological response of the
                                  The Basic ENT

patient must be carefully taken into account.

        The principal function of the larynx is not
speech as is commonly believed, but protection
of the airways. Speech is a purely coincidental
secondary benefit which has permitted us to
develop language, and indirectly culture, with
all its positive and negative consequences.

     Strictly speaking, dysphonia is any change
in the normal voice, and should include the
nasal voice of swollen adenoids or flue, the na-
sal escape of the cleft palate, or the ‘hot potato’
voice of epiglottitis, but usually we contemplate
only the causes that interfere with normal vocal
cord vibration. These are conveniently sepa-
rated into extralaryngeal and intralaryngeal.
                                     The Basic ENT


     Extralaryngeal causes are any that in-
terfere with the neural functioning of the
dynamic laryngeal structures. These include
psychogenic—a falsetto voice or a functional
aphonia. (This last is easily identified by asking
the patient to cough. A cough requires accurate
closure of the vocal cords and glottis while in-
trathoracic pressure is built up to be suddenly
released. If the patient coughs normally he
usually has no organic disease.)
     Neurological—any alteration in the func-
tioning of the recurrent laryngeal nerves or
the vagus, anywhere between the brainstem
and the larynx, or problems of coordination
originating in the cerebellum.
     Neuromuscular diseases, similarly can af-
fect laryngeal function.

    Far the most common of the pathological
causes is damage to the recurrent laryngeal
nerves, which wind a long and tortuous path
around the subclavian artery on the right and
the aorta on the left, to track back up along ei-
ther side of the trachea (in the sulcus between

the trachea and the oesophagus) to reach the
larynx. Since each nerve carries both adductor
and abductor fibres to the larynx, anastomosis
after damage is usually unsuccessful, for we
have no way even microscopically of aligning
the fibres accurately. The recurrent nerves are
easily damaged during thyroid surgery and
therefore any thyroidectomy technique re-
quires for the nerves to be carefully identified
and preserved. (The superior laryngeal nerve
may also be injured during thyroidectomy, near
the superior pole of the thyroid, and results in
a subtle dysphonia due to a slackening of the
vocal cords, which is however difficult to iden-
tify on laryngoscopy)
     Damage to a recurrent nerve paralyses the
vocal cord on the same side in the midline, so
that bilateral damage causes severe stridor
and usually requires a tracheotomy. (Unilat-
eral damage normally does not cause stridor
as the other vocal cord abducts sufficiently to
allow an adequate airflow)
     The left recurrent nerve is more commonly
paralysed than the right, for it descends into the
chest and may be stretched by cardiovascular
problems or involved in a bronchial carcinoma
or metastases. The right side may be paralysed
                                   The Basic ENT

by a thyroid tumour. Any vocal cord paralysis
without a history of thyroid surgery requires
careful exploration of the whole length of
the recurrent and vagus nerves to look for a
treatable cause. If the left cord is paralysed,
look for chest pathology!


     Anything interfering with the accurate ad-
duction or vibration of the vocal cords during
phonation will cause changes in the voice.
     The most obvious, affecting almost 50
% of the world population, is the hormone
(testosterone) dependent laryngeal growth in
boys during puberty, which induces periods of
dysphonia (breaking of the voice). Hypothy-
roidism causes both structural changes in the
laryngeal tissues and mucosa, and affects the
normal neurological functioning. The changes
are so subtle and gradual that they are often
not noticed by the patient or immediate family,
but reported by acquaintances who only see the
patient from time to time or speak with them
by telephone.
     Inflammatory causes are either acute;

during a cold or acute laryngitis or chronic due
to prolonged voice misuse or chronic infections
and smoking. Occasionally granulomatous dis-
eases such as tuberculosis, lepra or syphilis
cause changes of the larynx.
     Tumours may vary from the functional
vocal nodules, benign polyps and juvenile
papilloma, through to malignancies such as
carcinoma or lymphoma.
     The vocal nodules are due to chronic voice
abuse such as shouting and singing and are
typically seen at the junction of the anterior
1/3 with the posterior 2/3 of the vocal cords
(remember the mirror image is inverted); often
present bilaterally.
     Juvenile laryngeal papilloma are of viral
origin and often associated with genital con-
dyloma in the mother at the time of birth. They
generally present during early childhood with
progressive dysphonia and then stridor as the
papilloma cover the laryngeal structures and
gradually obstruct the airway. Treatment is
repeated careful removal of the papilloma with
electrocautery or laser, taking care to avoid
damaging the laryngeal structures, and avoid
bleeding as much as possible, as the papil-
loma may become implanted in any damaged
                                  The Basic ENT

mucosa. Tracheotomy is to be avoided at all
cost, since it is associated with extension to
the bronchial areas from which they are very
difficult to remove.
     The most common malignant tumour of
the larynx is carcinoma, and because of the
early presentation of dysphonia, the prognosis
of laryngeal cancer is almost as good as that
of skin carcinoma—as long as it is diagnosed
on time!—
     It is therefore essential in any patient,
especially a smoker, with dysphonia lasting
longer than 6 to 8 weeks, to make a diagnosis
preferably with biopsy if there are laryngeal

    Finally, dysphonia should not be confused
with other speech alterations such as dysar-
thria, aphasia and apraxia—look them up.

     The tonsils and adenoids, together with the
lingual tonsils and the lymphe follicles and con-
necting lymphe vessels, form part of Waldeyer’s
Ring; a continuous circle of lymphoid tissue
surrounding the upper air and food passages.
Its function is to produce antibodies against
the large number of antigens and pathogens
inhaled and ingested continuously with every
breath and swallow we take. Especially during
the first years of life. Gradually, as the number
of new antigens encountered decreases, the
lymphoid tissue atrophies into disuse. After
one or two years we have encountered the great
majority of the airborne antigens we are likely
to encounter during our lifetime, and the ad-
enoidal tissue, begins to atrophy from disuse,
                                        The Basic ENT

followed some years later by the tonsils (both
palatal and lingual)
     Occasionally, the lymphoid tissue presents
episodes of inflammation and hypertrophy
which we call tonsillitis or adenoiditis.
     Typically there is an initial viral upper respi-
ratory tract infection (sore throat, slight cough,
mild fever, runny nose) which starts to improve
after a few days, when there is suddenly a re-
lapse. The fever increases again and the sore
throat gets worse and there is dysphagia and
general malaise. The throat looks hyperaemic,
the tonsils red and swollen and often have white
spots where pus is draining from the tonsil-
lar crypts. The adenoids look similar, but are
hidden behind the palate and more difficult to
observe. Most tonsillitis infections are self lim-
iting over a week or two, but if severe, tend to
leave fibrosis and structural changes within the
tonsils which predisposes them to subsequent
infections. Antibiotic treatment should be care-
fully staged, for an antibiotic given during the
first 3 days of the viral infection will have little
effect except to change the bacterial flora of
the throat and induce strains resistant to the
particular antibiotic, so it will no longer be use-
ful if there is a secondary bacterial infection.

After the third day, if the patient experiences
the relapse of symptoms described above, an
adequate antibiotic will sometimes shorten the
illness by several several days. The antibiotic of
choice depends on the local bacterial resistance
patterns, and throat cultures may be taken to
aid in the choice. But normally a broad spec-
trum antibiotic (Co-Trimoxazol, an ampicillin or
a cephalosporin) is used, for the bacterial flora
of the throat is varied and often not sensitive to
a penicillin. Once started, the antibiotic should
be continued for at least 8 to 10 days, although
we re-evaluate the patient after three days, and
change the antibiotic if there has been no im-
provement. Thus, summing up: First three
days no antibiotics (symptomatic treatment
only). Then start on antibiotics for 8-10 days.
If there is not a considerable improvement in 3
days change the antibiotic. Throat cultures are
generally of little use for there is a large variety
of bacteria normally resident in the mouth and
throat. Fortunately, the dreaded ß-haemolytic
streptococcus which may cause lasting damage
to the heart (rheumatic fever) and kidneys, is
sensitive to any of the antibiotics mentioned
and to penicillin also.
     Surgery is usually decided on the basis
                                    The Basic ENT

of frequency of infections, not on the basis of
tonsil size. More than 5 severe episodes of ton-
sillitis per year requires tonsillectomy, while
less than that may be managed conservatively
with antibiotics. Tonsillar size in itself is not
a good indication, for the tonsils may be more
prominent or more embedded in the pharyngeal
mucosa and it is difficult to clinically evaluate
their exact size. A more useful parameter is
the degree of hyperaemia of the anterior tonsil
pillars (the mucosal fold partially covering the
      Adenoids, because of their strategic po-
sition in the upper airway, may obstruct the
nasal respiration if they become swollen or
hypertrophic, but take care not to equate all
nasal obstruction with adenoid enlargement,
for the nasal turbinates are far more often to
blame. Adenoidal size may be assessed by la-
ryngeal mirror, or lateral neck X-ray, but there
is a simple clinical technique for determining
if there is significant obstruction:
      Using two tongue depressors held together,
ask the patient to open his mouth and insert
them to carefully touch the soft palate just
above the uvula. The resting the lower tongue
depressor on the lower incisor teeth, ask the

patient to phonate a long Aaaaa, so that the
soft palate is elevated towards the posterior
nasopharyngeal wall. Carefully advance the
upper tongue depressor to again touch the
palate above the uvula, while the lower one
remains in place against the lower teeth. The
difference between the two tongue depressors
gives the mobility of the palate and is conven-
iently measured (for the sake of hygiene) on the
side which is not covered in saliva. Less than
5 mm is considered to be obstructive. (normal
is 8-10mm)

    Surgery for chronic tonsillitis is usually
carried out under general anaesthetic, and
consists in peeling the tonsil carefully out of
the mucosa and ligating or cauterising any
bleeding vessels. The adenoids if they are
enlarged are removed at the same time with
an adenoid curette. Tonsillitis is not a life
threatening disease, and tonsillectomy should
only be carried out by the specialist or under
supervision, for the tonsillar vessels are large
even in small children, and tend to bleed pro-
fusely, with possibility of a severe haemorrhage
or compromise of the airways which are life
threatening situations.
The Basic ENT

    Any persistent tumour in the neck should be
considered malignant unless proven otherwise.
Give the patient a short course of broad spec-
trum antibiotics first to rule out infective lymphe
glans, and check his Mantoux test. If these are
negative, it is best to use an aspiration biopsy
and cytology to make the diagnosis, rather than
compromise the subsequent treatment with an
excisional biopsy. Aspiration biopsy is one of
the major advances in the management of neck
tumours. It is easily carried out without anaes-
thetic, requires little equipment and has a fairly
steep learning curve. It has also been shown to
have an extremely low incidence of needle tract
metastases of malignant tumours. Obviously a
good cytologist or pathologist is required to in-
                                       The Basic ENT

terpret the slides, but once fixed they can be
posted anywhere for interpretation. The tech-
nique is simple and is described above with a
few useful variations.


        Thyroid nodules occupy a rather special
place among the neck tumours, for though they
are common all over the world, malignancies
occur in less than 20% for single nodules and
less than 10% for multinodular goitres. In-
discriminately operating on all of them would
lead to unacceptably high percentage of unnec-
essary thyroidectomies. Unfortunately, there
is no single clinical or laboratory finding which
will accurately distinguish between a benign
and a malignant nodule, so a selection must
be made on the basis of history and clinical
examination; requiring considerable skill and
experience on the part of the surgeon. Since
80% of thyroid carcinoma is of the Papillary
variety with a relatively ‘benign’ behaviour, a
little more flexibility, a certain amount of careful
observation is permissible. [Thyroid tumours

are of the 80%variety—80% benign, 80%pap-
illary carcinoma]
     Important clinical pointers are:
     1. Recent changes in size, shape , fixation
and hardness of the nodule.
     2. Associated lymphadenopathy, especially
in the Jugulo-omohyoid nodes.
     3. Dysphonia, dysphagia or stridor.
     4. Family history of thyroid disease.
     5. Patients aged less than 20 (half of all
single nodules found in children are malignant)
or more than 65 (more than 40 in males)

     Laboratory functions are of limited value,
since thyroid function tests are almost in-
variably normal. A Thyroid isotope scan where
available, will only differentiate between “hot”
and “cold” nodules, though it may often show
multinodular disease. Cysts however are iden-
tified as “cold” nodules, so that a Fine needle
aspiration should always precede the scan.
     The cyst is aspirated so the diagnostic
procedure is at once therapeutic. Small cysts
are only very rarely malignant and only require
repeated aspiration and careful observation.
Large cysts should be removed surgically.
     Otherwise, the patient with small nodules
                                    The Basic ENT

and cysts is given thyroid suppression therapy
with thyroxine and carefully observed. Should
he come into the above mentioned categories the
thyroid lobe is removed and sent to pathology.
There is much controversy surrounding partial,
subtotal and total thyroidectomy, for different
carcinoma, but great care should always be tak-
en not to injure the recurrent laryngeal nerves
and to leave at least one functional parathyroid.
Lack of thyroid hormone is easily treated with
thyroxine, but lack of parathyroid hormone is a
complex and difficult problem to deal with.

      A nasal fracture does not need an X-ray
                             for its diagnosis.

        An undeviated nasal fracture does not
                             require surgery.

    The nasal bones are covered by a thin
layer of skin on the outside and a thin layer
of mucosa on the inside, so it is not difficult
to determine by clinical exploration alone,
whether the bones are fractured. Special care
should be taken with the nasal septum which
is often displaced after a nasal trauma. We
usually have up to a week to reposition or re-
duce a nasal fracture, though the sooner it is
corrected, the better the results. Beware of a
septal haematoma; blood collecting between the
cartilage and the mucosa of the nasal septum,
                                       The Basic ENT

producing a round swelling projecting into the
nose on one or both sides and often blocking
the nasal respiration completely. As a rule,
the untreated haematoma infects, producing an
abscess which destroys the septal cartilage and
due to the shared venous network may result
in intracranial complications. The destruction
and absorption of the nasal cartilage produces
a collapse of the nose known as saddle nose or
boxer’s nose. Treatment of the haematoma is
simple and consists of aspiration with a large
needle, or a generous incision (approximately 1
cm in length) of the mucosa, to drain the hae-
matoma, or abscess if this has already formed,
and then packing the nose for a few days, to
prevent blood from collecting again.
      In severe facial trauma, carefully palpate
the orbital rims, and while fixing the forehead,
try to move the upper teeth and palate, to iden-
tify a possible facial fracture. The face usually
fractures according to the Lefort classification
(I, II or III). This is logical, because René Lefort
based his classification on experiments where
executed prisoners were thrown out of high
windows onto their faces, after which he dis-
sected them to find out where their faces had

    Treatment of a Nasal fracture.

        With the patient in a supine position,
the nose is carefully packed with cotton wool
soaked in 10% xylocaine spray and oxymetazo-
line drops. Care is taken to pack well into the
nasal vault, under the nasal bones, and as far
back as the tail of the middle turbinates. Subse-
quently 2% xylocaine solution with epinephrine
1 : 200,000. is infiltrated transcutaneously by
insulin syringe around the infraorbital, supra
and infratrochlear nerves, and along the nasal
dorsum for the external nasal branches. After
this it is important to wait for approximately 15
minutes while the anaesthetic takes effect. The
sensibility over the nose is then tested with a
needle and more anaesthetic is applied where
necessary. The dorsum of the nose is gently
massaged to reduce oedema and palpate the
fracture line
     The nasal pack is now removed and replaced
by a small length of gauze between septum and
inferior turbinate, to prevent any blood from
running back into the patient’s throat. This is
especially important if the procedure is done
under local anaesthesia.
                                     The Basic ENT

     Once the position of the dorsum is estab-
lished, the fracture may then be reduced by
simple digital pressure. No special instruments
are needed at this stage, and especially the use
of (medieval) Welsham’s or Asche’s forceps will
often produce more bruising of the subcu-
taneous and submucous tissues and epistaxis.
Any depression of the nasal bones is elevated
by means of straight Mayo scissors (which have
the ideal shape and are generally available in
any emergency department) inserted under the
nasal vault. The nasal septum is reviewed at
this stage and its position is corrected if nec-
essary with the Mayo scissors. If the fracture
is unstable, the nose is carefully packed with
gauze strip to stabilise the fragments internally
(both dorsal and septal). The nose is taped, to
reduce the subcutaneous oedema as much as
possible, and a small plaster of Paris splint ap-
plied to stabilise the nose externally. The pack
is removed after 2 to 3 days depending on the
degree of instability encountered during the
procedure. The splint remains in place for 5
days, and micropore is used for approximately
2 weeks.

     The difficulty or inability to swallow prop-
erly is always a serious complaint, which needs
to be analysed. If the patient claims to swallow
liquids more easily then solids we must exclude
a carcinoma or a stricture (is there associated
history of gastric reflux or achalasia? or swal-
lowing of foreign bodies, caustics or acids? ei-
ther by accident or as an attempted suicide?)
     Liquids causing more problems than solids
indicates a problem with swallowing co-ordi-
nation and is more often a neurological prob-
     Occasionally the patient complains of a
painless ‘lump in the throat’ which is felt on
swallowing but does not interfere with it. If
this is located in the neck, it may be a spasm
of the crico-pharyngeal muscle at the entrance
of the oesophagus due to a nervous or neurotic
                                     The Basic ENT

    Patients with severe tonsillitis, peritonsilar
abscess, pharyngitis, retropharyngeal abscess
or epiglottitis may also have difficulty swal-
lowing, but because of the severe pain (odyno-
phagia), rather than a physical or functional
    Persistent dysphagia, which shows no
improvement after some weeks needs to be di-
agnose more accurately by means of a barium
swallow and and endoscopic examination, with
biopsies of any abnormal looking area.

    Language is of basic importance. It is what
allows us to think rationally, to contemplate
past and future, it is what makes us human;
probabaly the only thing which differentiates
us from other animals.

     The normal child tends to start developing
speech by his first birthday (girls usually earlier
than boys) and it has been estimated that any
child with an IQ over 60 will be able to develop
     The innate language ability and the natural
drive to communicate is such that any group
of two or more persons will develop a language
even in isolation from other groups, and without
                                    The Basic ENT

a previous knowlege of a language. All lan-
guages are equally complex and can be learned
perfectly and without accent before the age of
10 or 12. This age limit is important for many
chidren suffer from secretory otitis media dur-
ing childhood; during the years when they need
all the auditory information they can acumulate
for language development
     If a child fails to develop language by the
age of two the reason must be determined.

    Verbal communication is a complex process
integrating hearing, thinking and speech.
    RECEPTION (ear) — PERCEPTION (hearing)
— INTEGRATION (higher cerebral functions)
— EXPRESSION (speech production)— VOICE
(Larynx function)

     The sequence is systematically explored.
     First we must ensure that the ear is func-
tioning. A secretory otitis media may produce
sufficient hearing loss to cause delayed speech
     Contrary to popular opinion, tongue tie
or short frenulum is very rarely the cause of
speech problems
The Basic ENT

Abducent 42
abscess 136
Accessory 45, 100
Acute otitis media 105, 107
Acute Suppurative Otitis Media 106
adenoidal tissue 39
Adenoids 152
adenoids 133, 149
air filled cavity 135
Airway problem 51
Allergic and angioneurotic oedema 60
allergic rhinitis 133
alveolar margins 33
aminoglycoside antibiotics 127
Amoebiasis 141
Ampicillins 137
angioneurotic oedema 60
anosmia 41
Anterior commissure 36
antibodies 149
aorta 144
aphasia 148
apraxia 148
Arnold’s Nerve 100
Arytenoids 36
aspiration biopsy 155
ataxia 116
atresia 62
auditory feedback 127
                                  The Basic ENT

auditory pathways 125
aura 140
auscultation 78

bacterial rhinitis 134
Balance 46
balance 116
Barber-Surgeons 14
barium swallow 164
Base of tongue 35
basket catheter 98
Bayonet / Tilley’s forceps 18
Bell’s Palsy 129
Bell’s sign 44
Benign (paroxysmal) positional vertigo 117
Bilateral palsy 64
biphasic stridor 55
     TRACT 75
Blind intubation 69
BPPV 117
Brain abscess 114
brain abscess 112
brainstem 27
breaking of the voice 146
bronchial carcinoma 76
buccal sulcus 33
bullous myringitis 104

Caloric Test 29
carcinoma 147
Central Vertigo 116

cerebellum 28
cerebral abscess 112
cervical headache 141
Chest X-Rays 78
Choanal atresia 57
choanal atresia 134
Cholesteatom 110
Chronic secretory otitis media 106
Chronic Suppurative Otitis Media 109
chronic suppurative otitis media 105
chronic voice abuse 147
Cluster headaches 140
Co-Trimoxazol 137
‘coffee ground’ vomitus 76
Conductive deafness 127
Conductive hearing loss 124
condyloma 147
congenital deafness 127
Coordination, 46
corneal reflex 43
corticosteroids 127
coug 144
cranial nerve palsies 116
cranial palsies 116
Cricothyroid (membrane) puncture 69
Croup 65
cysts 137
cytology 155

Deafness 123
deafness 116, 118
decongestant drops 137
                                    The Basic ENT

deep jugular nodes 40
Deep neck abscesses 67
dermatological 101
dermatological cream 103
deviation of the nasal septum 133
diabetic 103
Diagnostic set 17
dizziness 115
dysarthria 148
dysphonia 143, 147

ear discharge 116
Ear hook 18
ear surgery 129
Electro-Cautery 20
Embalmer-Surgeons 14
EMERGENCY Tracheotomy 70
endolymph 117
endoscopic examination 164
endotracheal tub 68
Epiglottis 36
Epiglottitis 60
ethmoid 135
Ethmoidal arteries 90
Eustachian tube 39, 105
exercises 120
expiratory strido 55
external carotid 90

external meatus 22, 102
Extradural abscess 114
Extralaryngeal dysphonia 144
eye diseases 13
eyes 116

Facial 100
Facial expression 129
Facial nerve 44
Facial nerve paralysi 114
facial pains 136
facial paralysis 111
facial plastic surgery 10
facial trauma 58, 160
False cords 36
falsetto voice 144
fasciculations 46
fishbone 96
flexible bronchoscope 98
Floor of mouth 33
fluctuating hearing loss 118
Fluid bubbles 23
Foley’s catheter 19, 87
Foreign bodies 63
Foreign bodies in the larynx 97
Foreign Bodies in the Nos 94
Foreign bodies in the throat 96
foreign body 67, 134
Foreign body in the oesophagus 98
Foreign body in the trachea and bronchi 98
fossae of Rosenmüller 39
foul smelling pus 137
                                       The Basic ENT

fractures of the temporal bone 129
frenulum 166
full blood count 77
function of the larynx 143
fundoscopy 42

gag reflex 45
gastric ulcer 76
genicular ganglion 44
Gentamicin 117, 118
Glaucoma 118
Glossopharyngeal 45, 100
glottis 62
Glue Ear 106
Granulomatous processes 63
Greater Auricular 100

H.Influenza 65
haematemesis 75
Haemophilus Influenza 60
haemoptysis 75
hair cells 126
Hallpike 30
hallucination of movement 119
Hard and soft palates 33
head                       mirror 17
Head lamp 17
head trauma 129
headache 116
hearing aid 128
Heimlich manoeuvre 97
Herpes Zoster 130
High Velocity VOR 29

higher cerebral functions 46
Hindu surgeons 14
Hinton 11
Historical Considerations 13
hoarseness 63
horisontal nystagmus 28
hormone 146
‘hot potato’ voice 60
Hypoglossal nerve 46
hypophysis 135
hyposmia 41
Hypothyroidism 146
hysterical aphonia 144

inferior and middle turbinates 31
inferior turbinates 38
inner ear 117, 125
inspiratory stridor 55
internal maxillary artery 89
IV catheter 19

Jacobson’s nerve 100
Jobson-Horne probe 18
juvenile papilloma 147

Kanamycin 118

Labyrinthine concussion 117
                                        The Basic ENT

Labyrinthitis 113, 114
labyrinthitis 117
language development 124
Laryngeal dysphonia 146
laryngeal mirror 14
Laryngeal mirrors 18
laryngeal papilloma 64, 147
Laryngo-tracheo-bronchitis (Croup) 65
laryngomalacia 59
larynx 40
Lateral Rectus muscle 43
Lefort 160
left recurrent nerve 145
left Recurrent nerve paralysis 64
Leonardo da Vinci 14
lepra 147
Lesser Occipital nerves 100
light reflex 22
Lingual nerve 44
lingual tonsils 149
lip-read 126
Little’s area 81
lump in the throat 163
lymphoid tissue 149

Malaria 141
Malignant otitis externa 103
Mandibular 43
Mantoux test 155
mastoid foramen 45
Mastoiditis 111, 114
Maxillary 43
maxillary 135

measles 126
mediastinal or pulmonary tumours 67
melaena 77
Meniere’s disease 117, 118
Meningitis 114
meningitis 112, 126, 141
metastases 67
middle turbinates 31
migrainous headache 140
movements 116
mucoid discharge 102
mucosa 32
mumps 126
Myringitis 104

nasal bones 159, 162
nasal cycle 133
nasal flora 136
Nasal packing 85
nasal polyp 134
nasal respiration 152
nasal secretions 32, 136
nasal septum 31, 159, 162
Nasal speculum 18
nasopharynx 38
nausea 116
nausea and vomiting 119
neck exercises 120
neck surgery 10
negative Rinne 25
Neoplasms 58, 63
neuroepithelium 113, 117
                                     The Basic ENT

neurological tests 29
neuroma of the acoustic nerve 117
Neuromuscular diseases 144
nonverbal human communication 129
nystagmus 28, 113, 116

Obstructive sleep apnoea syndrome 58
occipital lymph nodes 39
oculo-vestibular reflexes 28
Oculomotor 42
oesophageal varices 76
oesophagus 145
Olfactory nerve 41
Ophthalmic 43
Optic nerve 42
oral airway 68
organ of Corti 126
otic meningitis 112
Otitis externa 101
Otitis Media 105
Otolaryngology 10
otoliths 117
Otorhinolarynglogyheadandnecksurgery 10
Otoscope 17
otoscope 22
Ototoxic 117
Ototoxic drugs 118

Papillary 156
papilloedema 116

paranasal sinuses 135
Parasitic 141
parathyroid 158
parotid gland 39
Partial atresia 62
perforation 108
Peripheral Vertigo 116
photophobia 140
piracy 11
pneumatic bulb 23
Politzer 14
polyps 32, 137, 147
portal hypertension 78
positive Rinne 25
Post intubation stenosis 66
Post tracheotomy stenosis 66
Post-linguistic 124
posterior choanas 38
Posterior commissure 36
posterior labyrinth 127
posterior pack 87
posterior triangle 40
postnasal secretion 134
posture 116
Praeceptorum Optimum 47
pre and post auricular nodes 39
presbycusis 125
presbyopia 125
proprioceptive receptors 116
protection for the lungs 62
Pseudomonas 103
psychogenic 144
Pterygopalatine Fossa 88
Pulmonary blood 76
pulmonary tumours 67
                                      The Basic ENT

Pure Tone Audiometer 27
purulent rhinorrhoea 134

Recurrent Laryngeal Nerves 144
recurrent laryngeal nerves 144, 158
Referred pain 100
REM sleep 58
respiratory sclerom 60
Retromolar trigones 33
rheumatic fever 151
Rinne test 25
rigid bronchoscope 98
Rigid oesophagoscopy 100
‘rising sun’ sign 60
rock music 125
rotational vertigo 119

saddle nose 160
scan negative headache 139
Schrimer’s Test 44
scleroma 60
scotoma 140
secretions 23
Secretory otitis media 105
semicircular canals 117
sensation of rotation 115
Sensory neural hearing loss 125
Sensory-neural deafness 127
septal haematoma 159
serous labyrinthitis 113
silver nitrate 84
singing 147

Sinusitis 140
sinusitis 133
skin flora 101
sleep apnoea syndrome 58
Slüder headache 140
Smith Papyrus 14
smoker 63
sneezing 134
soft palate 153
soft palates 33
sphenoid 135
spinal cord 27
spiral ganglion 126
Spirit lamp 19
spontaneous nystagmus 29
spontaneous recovery 130
squamous debris 102
sternomastoi 39
Stethoscope 17
Streptomycin 117, 118
Stridor 55
stridor 147
subclavian artery 144
Subdural abscess 114
submandibular ducts 33
submandibular lymph nodes 39
submandibular salivary gland 39
submental lymph nodes 39
sudden onset hearing loss 127
superior laryngeal nerve 145
Superior Oblique muscle 43
superior turbinate 31
suppurative labyrinthitis 113
supraclavicular 40
                                  The Basic ENT

syphilis 147

Tagliacozz 14
Teeth 33
Temporomandibular joint 99
tension headache 141
The normal 21
the pathological 21
Throat cultures 151
thyroid carcinoma 156
thyroid gland 40
Thyroid nodules 156
thyroid suppression therapy 158
Thyroid tumours 67
thyroidectom 158
thyroidectomy 145
thyroxine 158
Tilley’s forceps 18
Tinnitus 125
tinnitus 116, 118, 125
Tongue 33
Tongue depressors 18
tongue tie 166
Tonsillar hypertrophy 58
tonsillar pillars 33
Tonsils 33
tonsils 149
Toothpullers 14
total deafness 126
Toynbee 14
trachea 145

tracheal rings 36
tracheostom 70
Tracheotomy 148
tracheotomy 145
transudate 136
trauma to the larynx 62
Treatment of a Nasal fracture 161
    TION 68
Trichloracetic acid 84
Trigeminal 100
Trigeminal nerve 43
Trochlear 42
tuberculosis 60, 76, 110, 119, 147
tuberculous otitis media 110
tumour 134
Tumours 147
tumours of the upper airway 61
Tuning fork 17
tympanic plexus 100

unilateral nasal discharge 94
Unilateral vocal cord paralysis 64
Upper airway problems 9
upper respiratory tract 101

vagal reflexes 119
Vagus 45, 100
vagus 144
Valleculae 36
Valsalva 14
vasomotor or viral rhinitis 133
                               The Basic ENT

Venous sinus thrombosis 114
vertical nystagmus 28
vertigo 28, 115, 118
vestibular labyrinth 27, 119
vestibular neuritis 117
Vestibular Neuronitis 119
vestibule 31
Vestibulo-Acoustic nerve 45
viral rhinitis 133
Visual Acuity 42
Visual fields 42
vocal cord paralysis 64
Vocal Cords 36
vocal nodules 147
voice production 62
vomiting 116

Waldeyer’s Ring 149
watch 26
Waters’ view 136
watery discharge 102
Watery rhinorrhoea 134
Wax in the Ear 92
The Basic ENT
The Basic ENT
The Basic ENT

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